Frailty in older adults is a common aging-related syndrome that can lead to adverse health outcomes. Although physical exercise and nutritional interventions have been widely recognized as beneficial for managing frailty, the comparative effectiveness of various intervention approaches remains uncertain. We systematically evaluated the effects of multicomponent exercise, nutritional supplementation, and combined interventions on frailty status and functional outcomes in older adults using network meta-analysis. Randomized controlled trials (RCTs) published between 2006 and 2025 were searched to include studies assessing the effects of multicomponent exercise, nutritional supplements (including amino acids and proteins, etc.), combined interventions, or standard care on frailty status in older adults aged ≥ 60 years. Changes in frailty scores constituted the primary outcome. Secondary outcomes comprised gait speed, the Short Physical Performance Battery (SPPB), and the Timed Up-and-Go test (TUG). Effect sizes were calculated using Standardized Mean Difference (SMD) and 95

Background Atherosclerosis (AS) is a chronic disease characterized by lipid deposition in the vascular intima. As the pathological basis of cardiovascular diseases, AS represents a major contributor to global morbidity and mortality. While Gualou Huoxue Jiedu Decoction (GHJD) has been widely used in clinical practice for the treatment of AS, the molecular mechanisms remain unclear. Purpose To investigate the anti-atherosclerotic effects and underlying mechanisms of GHJD. Methods ApoE-/- mice were treated with GHJD to evaluate its effects on plaque formation, lipid profiles, and inflammatory responses. The main compounds in GHJD were identified using UHPLC-Q-Orbitrap HRMS. Integrated analyses of network pharmacology, methyl-capture sequencing (MC-seq), and RNA-seq were performed to elucidate the molecular mechanisms of GHJD. In vitro experiments were conducted to validate its mechanism of action. Results GHJD alleviated plaque formation, improved lipid metabolism, and suppressed inflammation in vivo. Multi-omics analysis revealed that DNA methylation of Mfap4 could be a pivotal target of GHJD efficacy. In vitro assays confirmed that GHJD suppressed Mfap4 transcription and translation, leading to downregulation of integrin receptor family expression and inhibition of VSMC phenotypic switching. Conclusion GHJD exerts anti-atherosclerotic effects through epigenetic modulation of Mfap4 and downstream integrin/FAK signaling pathway, thereby inhibiting VSMC phenotypic switching. These findings provide pharmacological evidence supporting GHJD as a potential therapy for AS and, for the first time, validate MFAP4 as a pharmacological target, offering new insights into AS prevention and treatment.

Background:Atherosclerosis (AS) is a central pathological driver underlying most cardiovascular diseases. Gut microbiota and related metabolites participate in regulating atherosclerosis. Panax ginseng and Polygonum cuspidatum (GP) herb pair has traditionally been used for cardiovascular diseases. Some active compounds in GP have shown anti-atherosclerotic effects and the effects of GP still needs more evidence-based supports. Therefore, this study aims to investigate the potential effects of GP on atherosclerosis and explore the underlying mechanisms. Methods:Fifty C57BL/6J ApoE-/- mice were randomly assigned to five groups: model, statin, low-dose GP, medium-dose GP and high-dose GP. They were fed a high-fat diet (HFD) to induce atherosclerosis. Ten wild-type C57BL/6J mice were given chow diet and served as controls. After 12-week intervention, their aortic tissues were collected for Oil Red O staining, colon tissues for Alcian staining and immunofluorescence, and serum samples for measurement of lipid levels and inflammatory cytokines. Then, their fecal DNA was extracted for metagenomic sequencing, while cecum and ileocecal valves were for untargeted metabolomics. Finally, fecal microbiota transplantation was performed to assess the contribution of gut microbiota to observed effects. Twenty additional ApoE-/- mice were randomized to two groups: FMT-Mod and FMT-GPH, given feces from the model or high-dose GP group. Results:Atherosclerotic plaques accumulated in the aorta and aortic sinus after HFD, while statin and high-dose GP alleviated this burden. TC, TG, LDL-C, MCP-1, MCP-3 and IL-2 showed significant increase after HFD, while statin and GP decreased LDL-C, MCP-1 and MCP-3. The goblet cells, ZO-1 and Occludin decreased after HFD, while statin and GP increased them, indicating that the intestinal barrier integrity was improved. Additionally, the composition of gut microbiota was modulated by GP. Some candidate taxa were identified, such as Bifidobacteriales, Bacteroidetes and Escherichia coli. Twenty-two metabolites were differentially abundant among the control, model and GP groups. Nineteen of them were modulated by HFD and reversed by GP, including 1-methylnicotinamide, dopamine and lysoPA (0:0/18:0). Mice given fecal transplants from the high-dose GP group showed less aortic plaques, lower levels of some lipid and inflammatory cytokines, more goblet cells, more expression of ZO-1 and Occludin, and more 1-methylnicotinamide than those given fecal transplants from the model group. Conclusion:This study suggests that GP is beneficial for alleviating atherosclerosis in HFD-induced ApoE-/- mice, potentially by modulating the composition of gut microbiota and related metabolites.

Introduction:Atherosclerosis (AS) is driven by lipid accumulation, inflammation, and oxidative stress, leading to endothelial dysfunction and plaque formation. Emerging evidence indicates that iron overload and ferroptosis exacerbate these processes via enhanced lipid peroxidation and vascular injury. However, current Western medical strategies predominantly target lipid-lowering and inflammation, often overlooking iron dysregulation and ferroptotic pathways. Methods:We used ApoE-/- mice as an AS model and administered Tetramethylpyrazine (TMP), Paeoniflorin (PF), or their combination (TMP+PF). Serum lipids, oxidative stress biomarkers, iron metabolism indices, and ferroptosis-related markers were measured. Results:Both TMP and PF significantly reduced serum lipid levels and oxidative stress, normalized iron metabolism parameters, and suppressed ferroptosis-associated markers, indicating a protective effect against ferroptotic damage. Discussion:These findings suggest that TMP and PF mitigate AS by coordinately regulating oxidative stress, iron homeostasis, and ferroptosis. Their multi-targeted action may offer a complementary approach to conventional therapies, addressing the previously neglected mechanisms of iron-driven vascular pathology.

IntroductionWith the escalating global burden of population ageing, the comorbidity of geriatric coronary heart disease (CHD) and mild cognitive impairment (MCI) has emerged as a significant public health concern. This study aims to elucidate the underlying clinical disease features of MCI in elderly CHD patients through comprehensive multi-omics analyses and to establish a detailed phenomics profile.MethodsA cross-sectional study design will be implemented, enrolling 364 elderly patients diagnosed with CHD. Participants will be divided into MCI and cognitively normal groups based on Montreal Cognitive Assessment (MoCA) scores. Extensive data collection will include demographic characteristics, clinical parameters, laboratory investigations, and echocardiographic findings. These clinical data will be integrated with multi-omics analyses (including genomics, proteomics, and metabolomics) to identify differential biomarkers between the two groups.DiscussionThis study anticipates constructing an integrative network map delineating the multi-omics mechanisms underlying MCI in elderly CHD patients by correlating macroscopic clinical phenotypes with microscopic molecular characteristics. The findings are expected to provide a scientific foundation for early detection and intervention strategies. While acknowledging the inherent limitations of the cross-sectional design, future prospective studies are warranted to validate these findings. This investigation offers novel insights and potential therapeutic strategies for the prevention and management of comorbid CHD and MCI in the ageing population. This study has completed registration in the International Traditional Medicine Clinical Trial Registration Platform (ITMCTR2024000871).Clinical Trial Registrationhttps://itmctr.ccebtcm.org.cn, identifier ITMCTR2024000871.

Introduction Atherosclerosis (AS) is a chronic inflammatory disease characterized by the accumulation of plaque in the walls of arteries. Zhizi-Chuanxiong herb pair (ZCHP) is a traditional Chinese medicine formulation whose previous studies have demonstrated its inhibitory effect on AS. However, its underlying mechanisms remain unclear.Methods RAW264.7 cells were exposed to ox-LDL and treated with low or high-dose ZCHP, with or without the autophagy inhibitor 3-methyladenine (3-MA). We assessed lipid accumulation (Oil Red O staining, BODIPY-cholesterol assay), autophagic activity (immunofluorescence for LC3/LAMP1, transmission electron microscopy), and the expression of key autophagy and Wnt/beta-catenin pathway components (western blot, RT-PCR).Results ZCHP significantly inhibited ox-LDL-induced cellular lipid and cholesterol accumulation. Immunofluorescence and TEM revealed that ZCHP increased autophagosome formation and promoted autophagosome-lysosome fusion, which was impaired by ox-LDL. ZCHP increased the LC3-II/I ratio and Beclin 1 expression, while decreasing p62 expression. Furthermore, ZCHP also significantly decreased the mRNA levels of Wnt1, DVL1, beta-catenin, and Cyclin-D1. However, these effects were reversed by 3-MA.Discussion The protective effects of ZCHP are primarily mediated through the promotion of autophagic flux. The coordinated downregulation of the Wnt/beta-catenin pathway, which is dependent on functional autophagy, reveals a novel mechanistic insight into ZCHP's anti-atherosclerotic action. However, the study is limited by its in vitro design and the potential off-target effects of 3-MA, necessitating further validation in animal models.Conclusion ZCHP alleviates ox-LDL-induced macrophage injury by enhancing autophagy, an effect likely achieved through suppression of the Wnt/beta-catenin signaling pathway.

Ethnopharmacological Relevance:Chuanxiong (Ligusticum chuanxiong Hort.) and Chishao (Paeonia lactiflora Pall.) are widely used in Traditional Chinese Medicine (TCM) for their ability to promote blood circulation and resolve blood stasis, particularly in the treatment of cardiovascular diseases such as atherosclerosis (AS). Aim of The Study:This review systematically summarizes the potential mechanisms by which L. chuanxiong and P. lactiflora modulate iron metabolism, inhibit ferroptosis, and enhance blood flow, offering innovative strategies for the treatment of AS. Materials and Methods:A comprehensive literature search was performed using databases such as PubMed, Web of Science, and CNKI. We implemented a narrative review with explicit search strategies across regional databases that included specific keywords related to the pharmacological effects of Chuanxiong and Chishao, particularly their roles in iron metabolism and ferroptosis. Studies were selected based on predefined inclusion criteria, ensuring relevance and quality. The data were organized to summarize the mechanisms of action and therapeutic potential of these substances, while also incorporating insights from traditional medical texts, including classical TCM literature. Specific search strategy: SU=(("Atherosclerosis" [MeSH] OR "Atherosclerotic plaque" [Title/Abstract] OR "AS" [Title/Abstract] OR "Arteriosclerosis" [Title/Abstract]) AND ("Chuanxiong" [Title/Abstract] OR "Ligusticum chuanxiong" [MeSH]) AND ("Chishao" [Title/Abstract] OR "Paeonia lactiflora" [MeSH])) AND (("iron metabolism" [Title/Abstract] OR "ferroptosis" [MeSH] OR "lipid peroxidation" [Title/Abstract]) OR ("JAK-STAT pathway" OR "PI3K/AKT" OR "MAPK/NF-κB" OR "GPX4" [Title/Abstract]) AND ("randomized controlled trial" [Publication Type] OR "in vitro" [Title/Abstract] OR "in vivo" [Title/Abstract] OR "clinical study" [Title/Abstract])). Results:Ligusticum chuanxiong: and P. lactiflora modulate iron homeostasis by suppressing hepcidin and enhancing ferroportin, inhibit ferroptosis via GPX4 activation and System Xc- upregulation, and mitigate oxidative stress/inflammation through ROS scavenging and NF-κB suppression, collectively reducing atherosclerotic plaque instability. Conclusion:Chuanxiong and Chishao demonstrate significant potential as therapeutic agents for AS by targeting iron metabolism and ferroptosis. Their traditional use in TCM is supported by modern pharmacological evidence, highlighting their potential for integration into modern therapeutic frameworks.

Despite intensive glycemic control, diabetic cardiomyopathy (DCM) often progresses due to hyperglycemic memory (HGM), yet the specific cardiac cells perpetuating this injury remain unknown. To address this, we performed single-nucleus RNA sequencing (snRNA-seq) on hearts from an HGM rat model. Our analysis of 86,120 nuclei revealed HGM-specific inflammatory and epigenetic reprogramming signatures. Fibroblasts emerged as potential mediators, appearing to drive extracellular matrix remodeling via upregulated LAMININ and COLLAGEN signaling. We uncovered a distinct HGM-specific fibroblast subpopulation characterized by oxidative stress and H3K27 demethylation. Integrative analysis prioritized Fmo2 as a key pathogenic candidate, which was further supported via Mendelian randomization and clinical data as a putative causal gene. This study suggests that a pathogenic Fmo2+ fibroblast subpopulation may act as a pathological “memory carrier,” providing novel mechanistic insights and proposing exploratory therapeutic avenues for HGM-induced cardiac damage beyond glycemic control.

Chuanzhi Qingyu (CZQY) recipe is clinically used for the secondary prevention and treatment of cardiovascular diseases associated with atherosclerosis (AS) However, the potential active components and underlying molecular mechanisms require further elucidation. This study established a mouse model of vulnerable AS plaques through a high-fat diet. The efficacy of CZQY in stabilizing these vulnerable plaques was assessed using histological staining techniques. Additionally, biochemical analyses, ELISA assays, small animal ultrasound technology, and immunohistochemistry were employed. Subsequently, the active pharmaceutical ingredients of CZQY were identified through UPLC-Q-TOF-MSE. Finally, a network pharmacology approach, in conjunction with RNA-seq was utilized to predict the targets and mechanisms of CZQY in stabilizing vulnerable AS plaques, which were subsequently validated using Western blot and PCR methods. The research results show that CZQY can significantly improve lipid levels and liver function, reduce serum inflammation and oxidative stress levels, improve vascular function, and stabilize vulnerable AS plaques. The main components of CZQY that stabilize vulnerable AS plaques include flavonoids, terpenoids, and organic acids. The findings from RNA-seq and network pharmacology suggest that CZQY stabilizes vulnerable AS plaques potentially through mechanisms related to lipid metabolism, inflammatory responses, and cell migration, etc. Subsequent RT-qPCR and Western blot analyses confirmed that CZQY significantly modulated the expression of key targets at both mRNA and protein levels. In conclusions, CZQY effectively reduces risk factors associated with vulnerable AS plaques, improves vascular function, and stabilizes these plaques. This may be related to its ability to modulate mechanisms involving lipid metabolism, inflammation, extracellular matrix dynamics, and smooth muscle cell phenotype. These findings provide significant data support for further pharmacological research and clinical applications.

Objective:Hypertension remained an important public health problem with high morbidity and mortality and was emerging as a risk factor for future heart failure. The transition from hypertension to hypertensive heart disease (HHD) and heart failure grew progressively with time. Traditional Chinese medicine (TCM) has a history of several thousand years, where selected TCM for replenishing qi and activating blood circulation provides an alternative treatment for HHD. Methods:An extensive literature search was conducted across eight electronic databases from their inception until 8 September 2023, to evaluate the potential preventive effects of selected TCM as an adjuvant therapy on the progression of HHD. The outcome measures included blood pressure and indicators of cardiac structure and function under cardiac ultrasound. The mean difference (MD) and 95% confidence interval (CI) were used to determine continuous outcomes. Risk ratio (RR) with 95% confidence interval (CI) was used to determine dichotomous outcomes. The information about the overall certainty of the evidence from studies was presented according to specific outcomes using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) Guideline Development Tool (GDT) online software. Results:Twenty-one randomized controlled trials (RCTs) involving 2, 055 participants were included. Meta-analyses favored integrated Chinese botanical drugs and Western medicine on blood pressure, New York Heart Association classification, left ventricular ejection fraction, transmitral peak early diastolic velocity/peak late diastolic velocity ratio, left ventricular internal diameters, left ventricular mass index, interventricular septum thickness in diastole, and B-type natriuretic peptide compared with Western medicine alone. Results on cardiac output should be interpreted with caution due to sample size limitations. No severe adverse events were identified. Most of the Chinese botanical drugs originated from classical TCM formulas. The dosage form of Chinese botanical drugs was oral. Salvia miltiorrhiza Bunge (Danshen), Oreocome striata (DC.) Pimenov & Kljuykov (Chuanxiong), Pueraria montana var. lobata (Willd.) Maesen & S.M.Almeida ex Sanjappa & Predeep (Gegen), Astragalus mongholicus Bunge (Huangqi), and Typha angustifolia L. (Puhuang) were the top 5 Chinese botanical drugs, which might be associated with replenishing qi and activating blood circulation. Conclusion:Selected TCM had the potential to be effective as an adjuvant therapy for alleviating adverse left ventricular remodeling and improving cardiac function after HHD, and therapy of replenishing qi and activating blood circulation may serve as a potential reference for treatment. To better assess Chinese botanical drugs' preventative effects, more long-term, high-quality RCTs are still necessary. Systematic Review Registration:https://www.crd.york.ac.uk/PROSPERO/#myprospero, identifier CRD42022346030.

DNA methylation plays a critical role in myelodysplastic syndrome (MDS). Here, we aimed to observe the effects of polydatin (PD) on DNA methylation in MDS cells on a genome-wide scale and explore the underlying mechanisms, providing new evidence for PD as a novel hypermethylation agent. We used the Gene Expression Omnibus (GEO) online database to evaluate the DNA methylation characteristics of MDS patients. A Human Methylation 850 K BeadChip was used to evaluate the effects of PD on DNA methylation in SKM-1 cells. Western blotting (WB) was used to observe changes in the expression of related proteins. Cytoscape was used to determine the key genes that were hypermethylated by PD. The therapeutic effects were evaluated using flow cytometry experiment and a cell counting kit-8 (CCK-8) assay in vitro. Data from the GEO online database revealed that aberrant gene hypomethylation plays an important role in MDS. In MDS cells, 448 genes (71.91%) were hypermethylated following PD treatment. These hypermethylated genes are related to cancer-related signaling pathways. Moreover, key hypermethylated genes, including PIK3CA, ITPR3 and SPOPL, were identified, and these three genes are all oncogenes. Most importantly, PD decreased the protein expression of the above three oncogenes. Finally, we found that PD could inhibit the proliferation of MDS cells, arrest them in the S phase and induce their apoptosis. Our findings demonstrated that PD has therapeutic effects on MDS by inhibiting the protein expression of oncogenes via hypermethylation in vitro, indicating that PD may be a novel hypermethylation agent.

PURPOSE:This study aims to explore the mechanism of Bazi Bushen Capsule (BZBS) in treating skin laxity by combining network pharmacology and clinical research. METHODS:The active ingredients and potential drug targets of BZBS were obtained from TCMSP, TCMBANK, and SuperTCM databases. The potential disease targets of skin laxity were obtained from GeneCards, OMIM, and DisGeNET databases. The common core targets and key compounds were determined using Cytoscape software to construct the Drug Key Compound-Target network and Protein-Protein Interaction network. The mechanism of BZBS in treating skin laxity was revealed by Gene Ontology and KEGG enrichment analysis. Subsequently, to further verify the analysis results, a prospective single-group clinical trial was conducted, including 35 female volunteers with skin laxity. The planned study visits were initially scheduled for a 12-week period. The volunteers' average depth of skin wrinkles, skin elasticity parameters, and skin moisture content were examined at 0 week before the experiment and 12 weeks after the experiment. RESULTS:Network pharmacology shows that key compounds are quercetin, kaempferol, arachidonate, suchilactone, ammidin, deoxyharringtonine, sitosterol, mandenol, ethyl linolenate, stigmasterol, poriferast-5-en-3beta-ol, and cholesterol; core targets include AKT1, IL6, TP53, TNF, EGFR, TGFB1, JUN, MMP9, MTOR, and MMP2; the Relaxin, MAPK, PI3K-Akt, JAK-STAT signaling pathways, and cellular senescence may be the main ways for BZBS in treating skin laxity. After BZBS treatment, the average wrinkling depth of the enrolled volunteers decreased, and the skin elasticity and moisture content increased. CONCLUSION:BZBS may treat skin laxity by repairing the mucosal barrier, regulating protein metabolism, and showing good therapeutic effects. TRIAL REGISTRATION:WHO-recognized clinical trial registry: ChiCTR2200058262.

Atherosclerotic cardiovascular disease (ASCVD) continues to increase globally as the most common cardiovascular disease. Lifestyle and metabolic risks are major contributors to the increase in the burden of ASCVD. However, the epidemiological characterization of the burden of ASCVD due to lifestyle and metabolic risks has not been adequately documented. We analyzed data from the 2021 Global Burden of Disease Study to assess the disability-adjusted life years (DALYs) and age-standardized DALY rate (ASDR) attributed to ASCVD induced by lifestyle and metabolic risks. This study also analyzes temporal trends and inequalities in disease burden. Lifestyle and metabolic risks led to an increase in the DALYs and a decrease in the ASDR for ASCVD. High systolic blood pressure (SBP) was the primary contributor to the burden of ischemic heart disease (IHD) and ischemic stroke (IS), whereas high fasting plasma glucose (FPG) was the primary contributor to the burden of peripheral artery disease (PAD). High FPG and high body mass index (BMI) are primary risk factors that contribute to a more rapid increase in the burden of ASCVD. Over 32 years, high SDI regions reduced ASCVD burden linked to lifestyle and metabolic risks, while low SDI regions saw increases. ASCVD attributable to lifestyle and metabolic risks remains a major global public health concern. Although the burden of ASCVD caused by lifestyle and metabolic risks has improved in developed countries, developing countries still need to take effective measures to reduce the disease burden. Furthermore, while high SBP remains the leading contributor to the ASCVD burden, it is also crucial to recognize that high FPG and high BMI are becoming significant drivers of the growth in the ASCVD burden. This highlights the need for a paradigm shift in ASCVD prevention and control strategies-from single risk management to comprehensive metabolic network regulation.

Panvascular aging offers a pivotal theoretical basis that accelerates the translation of basic scientific research into clinical practice, specifically for the prevention and treatment of cardiovascular comorbidities in the elderly. This biological process is distinguished by two core, interdependent features. In the temporal dimension, it presents as a gradual, age-associated decline in vascular structure and functional integrity. In the spatial dimension, it manifests as synchronous vascular damage across multiple organ systems, including the heart, brain, lungs, kidneys, and peripheral vessels. Critically, the progression of panvascular aging is not a passive process but is tightly modulated by a complex, dynamic regulatory network within the panvascular microenvironment, where various molecular and cellular factors interact to shape vascular aging trajectories. This paper begins with a systematic overview of the fundamental connotation of panvascular aging, clarifying its theoretical framework, and then elaborates on its multiple typical manifestations that collectively contribute to its pathological phenotype. Subsequently, the study focuses on the latest research progress regarding the role of the panvascular microenvironment in driving vascular aging, with particular emphasis on key regulatory elements (residual cardiovascular risk, intrinsic vulnerability factors, and chronic inflammatory responses). Concurrently, it dissects the pathological links between panvascular aging and major cardiovascular comorbidities, including cardio-cerebral comorbidities (e.g., coronary heart disease combined with ischemic stroke), cardio-metabolicrenal syndrome (interactions between cardiac dysfunction, metabolic disorders, and renal impairment), cardio-peripheral vascular comorbidities (e.g., heart failure with peripheral arterial disease), and cardio-pulmonary comorbidities (e.g., coronary artery disease with chronic obstructive pulmonary disease). Furthermore, the paper identifies and discusses current bottlenecks in the field: limitations in fully elucidating the cross-organ regulatory mechanisms of panvascular aging, and challenges in translating mechanistic findings into effective clinical interventions. To address these gaps, it proposes three targeted strategies: establishing a panvascular aging risk stratification and early warning model to enable precise risk assessment in elderly populations; developing an integrated early identification system for panvascular aging that combines principles of traditional Chinese medicine, Western medicine, and digital intelligence; and constructing a multidisciplinary integrated platform for the prevention and treatment of panvascular aging, and data scientists to optimize care for elderly patients with cardiovascular comorbidities. Looking forward, future research in this domain will focus on three core objectives: integrating spatial and temporal mapping techniques to visualize the dynamic, organ-specific progression of panvascular aging; identifying and validating cross-organ regulatory targets that govern vascular aging; and developing novel, targeted therapeutic agents that address the root causes of panvascular aging-related comorbidities, ultimately providing more effective, personalized strategies for managing cardiovascular diseases in the elderly.

With the evolving landscape of diseases, heart failure with preserved ejection fraction (HFpEF) now encompasses more than half of all heart failure patients. This condition is clinically diverse, involving multiple organ systems and often occurring alongside the aging process. To deeply investigate the common pathogenesis of HFpEF and to explore new therapeutic approaches is of great significance for the treatment of HFpEF. Epicardial adipose tissue (EAT) is not only a dynamic organ with biological functions but also physically adjacent to the myocardium and coronary arteries, endowing it with unique properties as a visceral fat depot. During pathology, EAT can secrete adipocytokines via paracrine mechanisms, establishing direct communication with the heart and vascular, thereby impacting cardiac function. This review aims to elucidate the intricate relationship between EAT and cardiac function in HFpEF, delineate the roles of adipocytes, macrophages, lymphocytes, and stem cells within EAT in HFpEF, and summarize the progress in research regarding drug therapies targeting EAT for HFpEF treatment.

Myocardial infarction (MI) ranks among the leading causes of death globally, with its prognosis closely linked to inflammatory responses. Both excessive early inflammation and persistent residual inflammation lead to adverse cardiac remodeling and heart failure. In recent years, the role of trained immunity in cardiovascular risk factors and MI-associated inflammatory responses has garnered increasing attention. Cardiovascular risk factors can induce trained immunity, placing the body in a “preactivated” innate immune state prior to MI occurrence. This state is further amplified upon myocardial necrosis, triggering excessive inflammation. Additionally, MI itself can induce trained immunity, leading to long-term inflammatory memory and residual inflammation risk. Targeting metabolic and epigenetic pathways of trained immunity offers approaches for post-MI anti-inflammatory interventions. A comprehensive understanding of trained immunity’s mechanisms in MI holds promise for establishing theoretical foundations and translational directions for precision anti-inflammatory therapies and improving long-term patient outcomes.

背景 老年高血压合并认知障碍已经成为全球公共卫生问题之一，系统评价我国老年高血压患者轻度认知障碍(MCI)患病率，有助于为防治老年高血压人群的认知损伤提供数据参考。目的 采用Meta分析的方法评价我国老年高血压患者MCI患病率，并进一步探讨患病率的发展趋势。方法 系统检索中国知网、万方数据知识服务平台、维普网、中国生物医学文献数据库、PubMed、Cochrane Library、Embase、Web of Science中英文数据库，检索时间自建库至2024-02-22，采用NoteExpress软件进行文献管理和筛选，采用美国卫生保健质量和研究机构(AHRQ)横断面研究评价标准进行文献质量评价，由2名研究者独立筛选文献，提取数据并评价纳入文献质量，StataMP 14.0软件进行Meta分析和亚组分析。结果 系统分析了2008—2023年27篇横断面研究，共涉及老年高血压患者57 461例，其中患MCI 11 812例。通过随机效应模型进行Meta分析，高血压患者MCI总体患病率为21.3%(95%CI=18.4%～24.2%,P<0.001)。纳入研究文献共涉及我国11个省(区、市)，各省(区、市)间及地理区域间患病率差异较大；2008—2023年老年高血压MCI患病率随时间呈波动上升趋势，整体患病率均超过10%。亚组分析结果显示：我国农村老年高血压患者MCI患病率为33.6%(95%CI=6.4%～60.7%,P<0.001)，城市患者患病率为21.8%(95%CI=18.1%～25.4%,P<0.001)；华北地区患病率(14.0%,95%CI=9.3%～18.7%,P<0.001)较其他地区低。简易精神状态检查量表(MMSE)+蒙特利尔认知评估量表(MoCA)联合应用评估的MCI患病率为25.9%(95%CI=15.8%～36.0%)，单一MoCA评估的MCI患病率为21.4%(95%CI=18.5%～24.4%)，单一MMSE评估的MCI患病率为17.9%(95%CI=13.9%～21.9%)。结论我国老年高血压患者MCI总体患病率较高，不同省市、城乡间患病率存在较大差异，并随时间呈波动上升趋势，不同评估工具的MCI检出率存在一定差异，受文献研究数量和异质性影响，结论尚需进一步高质量研究证实。

Contemporary renowned practitioners of traditional Chinese medicine(TCM)have developed a systematic theoretical framework and accumulated extensive clinical experience in the treatment of cardiac arrhythmia.By systematically organizing the academic perspectives of 28 contemporary TCM masters and selecting 50 high-quality studies from a pool of 545 related documents,this study conducted an in-depth analysis of the etiology and pathogenesis,diagnostic approaches,treatment principles,and characteristics of medication.Regarding the understanding of etiology and pathogenesis,contemporary TCM experts generally regard arrhythmia as a syndrome characterized by a root deficiency and superficial excess,often presenting as a complex of both deficiency and excess.The root deficiency primarily involves insufficiency of Qi,blood,Yin,and Yang,while the superficial excess often manifests as obstruction due to phlegm turbidity and blood stasis.In terms of diagnosis,emphasis is placed on syndrome differentiation through the comprehensive application of the four diagnostic methods,particularly valuing the clinical utility of pulse diagnosis,and stressing the organic integration of disease differentiation with syndrome differentiation.Treatment is guided by the core principles of holism and syndrome differentiation,with a focus on harmonizing the Zang-fu organs and reinforcing the root to nourish vital Qi.Therapeutic methods such as resolving phlegm and stasis and combining elimination with tonification are applied flexibly.The prescription and use of medicines are characterized by adaptability,simplicity,and significant efficacy,reflecting a faithful adherence to the essence of TCM theory while actively incorporating insights from modern medicine.This demonstrates an academic pursuit of preserving tradition while fostering innovation.The study indicates that the formation of these academic features is influenced by multiple factors,including the historical context,regional environments,policy support,and mentorship inheritance.These characteristics reflect the innovative development of contemporary TCM on the foundation of tradition,integrating both TCM and western medicine,with distinct features and notable clinical efficacy,thereby providing important references for the TCM-based diagnosis and treatment of cardiac arrhythmia.

Coronary artery disease (CAD) remains a significant global health burden, profoundly impacting both physical and mental well-being. Psychocardiology underscores the critical influence of psychological factors on the development, diagnosis, and management of cardiovascular diseases. Patients with CAD frequently experience high rates of depression and anxiety, which are closely linked to mental stress-induced myocardial ischemia, cognitive impairment, and delirium. Given that cognitive decline and delirium severely compromise patient prognosis, targeted interventions and standardized care are essential. To address these needs, the Psychocardiology Medicine Branch of Chinese Medical Association Beijing Branch and the Psychocardiology Education Professional Committee of China Medical Education Association, together with over 50 experts from 40 organizations, have developed these association standards (No. T/CAS 812-2024). This December 2025 update provides a refined framework for the clinical diagnosis and treatment of CAD complicated by depression, anxiety, and cognitive impairment. These guidelines aim to direct standardized clinical practice and improve the overall physical and psychological prognosis for this high-risk population.

Background Perimenopause represents a pivotal transitional phase in female reproductive ageing, characterized by a marked decline in estrogen levels and a concomitant surge in cardiovascular disease (CVD) risk. With the global perimenopausal female population exceeding 850 million and continuing to expand due to demographic ageing, understanding the long-term trends and regional disparities in CVD burden among this group is critical. However, a comprehensive analysis of these patterns remains lacking. Methods Utilizing data from the Global Burden of Disease (GBD) 2021 study, we examined CVD-related deaths and disability-adjusted life-years (DALYs) among perimenopausal women across 204 countries and territories from 1990 to 2021. Joinpoint regression models were employed to assess temporal trends via average annual percentage change (AAPC), while regional variations were evaluated based on socio-demographic index (SDI) and geographic location. Results Global Trends : Between 1990 and 2021, CVD-related deaths among perimenopausal women rose from 334,000 to 414,000 (AAPC = 0.71%), while DALYs increased from 14.23 million to 18.39 million (AAPC = 0.84%), with notable fluctuations in 1998 and 2003. SDI Stratification : Medium-SDI regions bore the highest burden (145,000 deaths, 6.46 million DALYs in 2021), whereas high-SDI areas exhibited a declining trend (26,000 deaths, 1.29 million DALYs in 2021). Age and Regional Differences : The 50–54-year age group experienced the steepest rise in CVD burden. Oceania recorded the highest mortality increase (AAPC = 2.46%), while South Asia had the highest absolute death toll (249,000). Disease Spectrum : Ischemic heart disease (IHD) and stroke dominated, accounting for 82.7% of deaths and 81.6% of DALYs. Atrial fibrillation showed the fastest mortality growth (AAPC = 2.11%), while Rheumatic heart disease (RHD) DALYs declined significantly (AAPC = -0.63%). Conclusions The global CVD burden among perimenopausal women continues to escalate, disproportionately affecting low-to-middle SDI regions and women aged 50–54. Targeted, gender-sensitive prevention strategies—particularly for Ischemic heart disease (IHD) and stroke—are urgently needed to mitigate disease burden in high-risk populations.