Cardiorenal syndrome (CRS) is a pathological condition characterized by the synergistic deterioration of cardiac and renal function. This review attempts to systematically elucidate the pathophysiological mechanisms of CRS from the perspective of intercellular communication between cardiac and renal cells. We first analyze the characteristics of communication between the heart and kidneys under physiological conditions and then describe the pathological communication pathways mediated by intercellular communication (such as soluble factors and extracellular vesicles) in cardiorenal syndrome. We then provide a detailed analysis of the unique communication features observed in different subtypes of CRS. Based on this, we reinterpret the role of existing therapies in regulating cardio-renal cell communication and propose potential targeted strategies, including extracellular vesicle therapy and microRNA (miRNA)-targeted delivery systems. Finally, we discuss the challenges facing this field and future research directions, with the aim of providing new insights into the mechanisms and treatment of CRS.

White matter degeneration in aging drives cognitive and motor decline. Oligodendrocytes (OLs) and their precursors are central to this process. Their intrinsic aging, marked by differentiation failure, metabolic and mitochondrial deficits, and transcriptional epigenetic dysregulation, causes myelin thinning and axonal support loss. Degeneration is amplified by dysfunctional crosstalk: microglia clear debris poorly and turn inflammatory; astrocytes disrupt lipid balance and secrete inflammatory signals; vascular defects impair metabolic supply; and T cell infiltration injures OLs. We review therapies targeting OL lineage, glial networks, vascular health, and lifestyle. Positioning OLs as integrative hubs of white matter integrity offers new strategies to maintain brain function during aging.

Background:High mortality and prevalence rates are hallmarks of chronic heart failure (CHF). Patients frequently have a much lower quality of life as a result of diminished exercise tolerance. Chinese guidelines have recommended Yiqi Fumai lyophilized injection (YQFM) for the treatment of heart failure, although there is currently inadequate evidence to support its effectiveness in increasing exercise tolerance in these patients. Objective:The purpose of this cohort study is to examine the relationship between the improvement of exercise tolerance in patients with CHF and the addition of YQFM to guideline-directed medical therapy. Methods:In total, 216 hospitalized patients with CHF with New York Heart Association (NYHA) functional classes II-IV were to be enrolled in the prospective, observational cohort trial design. The participants were divided into a YQFM group (exposed group: n=144) and a non-YQFM group (nonexposed group: n=72) at a 2:1 ratio based on real clinical medication and patient preference. Standard guideline-directed medical therapy was administered to both groups; however, the YQFM group also got a 10-day YQFM exposure. The change in metabolic equivalents measured by the Veterans Specific Activity Questionnaire was the main outcome. The 6-minute walk distance, Kansas City Cardiomyopathy Questionnaire score, NYHA functional class, N-terminal pro-B-type natriuretic peptide levels, and echocardiographic parameters were among the secondary objectives. Traditional Chinese medicine syndrome scores and the frequency of hard clinical occurrences were the exploratory objectives. A linear mixed-effects model was used to examine repeated measurement data, and propensity score weighting was used to account for baseline confounding variables. Results:The first patient was registered in June 2024, and all 216 patients had been recruited and followed up with by December 2025. Data cleaning and statistical analysis began in January 2026, with final results scheduled to be published in the autumn of 2026. Conclusions:This study, using a prospective cohort design, intends to offer high-quality, real-world evidence for the use of YQFM in cardiac rehabilitation for heart failure. This will aid in the optimization of preventative and treatment strategies for CHF that combine traditional Chinese and Western medicine, giving an objective basis for enhancing patients' long-term quality of life.

BACKGROUND:Epidemiological data indicate a significant global increase in both comorbidity and mutually induced rates between cardiovascular and neurological diseases. Among these, cardiovascular and cerebrovascular diseases share eleven co-localized loci. The critical role of the brain-heart axis in these processes has been increasingly recognized. This axis mediates dynamic bidirectional crosstalk via neuroendocrine, neuroimmune and related pathways, with key mediators including the hypothalamic-pituitary-adrenal (HPA) axis, gut-derived metabolites, extracellular vesicles (EVs), and autonomic nervous system (ANS). Conventional siloed care across cardiology and neurology specialties, alongside single-organ targeted therapies, fails to effectively disrupt the pathological vicious cycle of brain-heart interactions. Targeting key mediators of the brain-heart axis holds significant clinical potential for the treatment of neurological or cardiovascular diseases. AIM OF REVIEW:This review systematically summarizes the key advances in brain-heart crosstalk over the past decade, delineates the direct neural pathways and indirect regulatory mechanisms between the two organs. Against this backdrop, we outline the clinical potential of nervous system-targeted strategies for cardiac disease and related neurological complications, alongside the broad promise of cardiac function optimization to modulate immune and endocrine pathways for cardio-cerebral comorbidity management. KEY SCIENTIFIC CONCEPTS OF REVIEW:We discuss the mediators underlying brain-heart crosstalk, and delineate the distinct functional roles of the brain-heart axis across diverse cardiovascular diseases and psychiatric disorders, offering new conceptual frameworks for treating cardiocerebral comorbidities.

Background: Chronic Cardiorenal Syndrome (CRS types 2/4) involves the mutual exacerbation of heart failure and chronic kidney disease, with over half of heart failure patients affected by renal impairment that increases mortality and rehospitalization. Despite advances in management, prospective evidence for Traditional Chinese Medicine in chronic CRS is lacking. Qishen Yiqi Dropping Pills (QSYQ) have proven safe in cardiovascular care, but their concurrent renoprotective effects remain unconfirmed. Based on preliminary cardiorenal protective findings, this study evaluates QSYQ combined with standard therapy on symptoms, function, biomarkers, and outcomes in chronic CRS. Methods: This is a prospective, multicenter, observational cohort study. Patients will be stratified into two groups based on whether or not they receive QSYQ treatment: an "Exposure Group" (standard background pharmacotherapy plus QSYQ; n=60) and a "Non-exposure Group" (standard background pharmacotherapy alone; n=60). The study duration is 270 days, with the exposure period set to the initial 90 days. Follow-up assessments will be conducted at baseline, and on days 90, 120, 180, and 270. The primary outcome measure is the 6-Minute Walk Test (6MWT). Secondary outcome measures include the New York Heart Association (NYHA) functional classification, N-terminal pro-B-type natriuretic peptide (NT-proBNP), serum creatinine (Cr), blood urea nitrogen (BUN), estimated glomerular filtration rate (eGFR), C-reactive protein (CRP), trimethylamine N-oxide (TMAO), major adverse renal and cardiovascular events (MARCE), the Veterans Specific Activity Questionnaire (VSAQ), and the Kansas City Cardiomyopathy Questionnaire (KCCQ). Throughout the entire study period, adverse events will be recorded to facilitate safety assessments. Discussion: This study will comprehensively assess QSYQ's clinical utility for chronic CRS, evaluating functional capacity, quality of life, biomarkers, and long-term outcomes to provide prospective evidence for integrating Traditional Chinese Medicine into chronic CRS management.

Ischemic heart disease is a leading cause of global morbidity and mortality, yet early diagnosis and targeted therapies remain limited. Exosomes, small extracellular vesicles carrying nucleic acids, proteins, and lipids, mediate intercellular communication and show promise for diagnostic and therapeutic use due to their stability, biocompatibility, and targeted delivery. Circulating exosomal profiles reflect myocardial pathology, enabling early detection, risk stratification, and monitoring. Exosomes from mesenchymal stem cells, immune cells, endothelial cells, and other stem cells exert cardioprotective effects. This review summarizes advances in exosome-based diagnostics and therapies and highlights their potential as biomarkers and innovative treatments.

Background:Coronary artery disease (CAD) remains a leading cause of global mortality and disability. CAD patients face tradeoffs between antithrombotic therapy benefits and bleeding risks, underscoring the need to incorporate patient values and preferences into clinical guidelines. Establishing minimal important differences (MIDs) for patient-important outcomes supports clinical guideline development by determining the smallest change in outcomes that patients consider important. However, directly conducting patient surveys to establish MIDs presents several methodological challenges. Methods:We established a multidisciplinary working group to guide the MID investigation. Using a three-phase process, we identified key outcomes through literature review and discussion. We will develop draft health outcome descriptions by synthesizing evidence from clinical guidelines and qualitative studies, supplemented with patient interviews, and refine the drafts through iterative cognitive interviews. We then designed outcome-specific draft MID questionnaires and will employ cognitive interviews to assess clarity and comprehensibility. Discussion:This study will develop standard materials for surveying patient values and determining MIDs in Chinese CAD patients. The resulting methodology will support future investigations into patient-important outcomes and provide critical evidence for clinical guideline development.

OBJECTIVE:To elucidate the mechanism of Yiqi Fumai Formula (YQFM) in acute decompensated heart failure (ADHF) via the Nrf2/SLC7A11/GPX4 pathway in regulating ferroptosis. METHODS:Network pharmacology was employed to predict the underlying mechanisms of YQFM in ADHF. Rat models of ADHF were established, incorporating agonists or inhibitors of key ferroptosis pathways. The therapeutic mechanism of Yiqifumai Formula was investigated by assessing cardiac structure/function, myocardial injury biomarkers, lipid peroxidation, iron metabolism, ultrastructural changes, and key ferroptosis pathways. RESULTS:Network pharmacology analysis suggested that YQFM might intervene in ADHF by modulating key processes of ferroptosis, including lipid metabolism, inflammatory response, and cell survival. Experimental validation confirmed that YQFM improved cardiac function, reduced myocardial lipid peroxidation, and inhibited cardiomyocyte ferroptosis in rat models. This cardioprotective effect is likely associated with the regulation of the Nrf2/SLC7A11/GPX4 signaling pathway. CONCLUSION:YQFM exerts the cardioprotective effect in ADHF by suppressing ferroptosis through the modulation of the Nrf2-SLC7A11/GPX4 pathway.

Mitochondrial homeostasis is essential for cardiomyocyte survival and optimal cardiac function. Recent studies have revealed that novel forms of programmed cell death—including ferroptosis, cuproptosis, pyroptosis, necroptosis, NETosis, and disulfidptosis—interact closely with mitochondrial quality control mechanisms, such as mitochondrial dynamics and mitophagy. This review provides a comprehensive overview of the molecular pathways underlying mitochondrial fusion, fission, and selective autophagic clearance, and highlights how disturbances in these processes contribute to cardiovascular disease progression. We further discuss the crosstalk between each form of programmed cell death and mitochondrial quality control, emphasizing the bidirectional influence whereby mitochondrial dysfunction can sensitize cardiomyocytes to cell death, while cell death pathways exacerbate mitochondrial injury. Mechanistic insights are provided for ferroptosis-driven lipid peroxidation, cuproptosis-associated copper dysregulation, pyroptotic inflammasome activation, necroptotic receptor-interacting signaling, NETosis-mediated oxidative stress, and disulfidptosis-induced cytoskeletal collapse. By integrating these findings, we identify critical regulatory nodes and molecular hubs that represent potential therapeutic targets to preserve mitochondrial integrity and prevent cardiomyocyte loss. Finally, we discuss emerging strategies for modulating these pathways and outline future research directions to clarify the interplay between mitochondrial homeostasis and novel programmed cell death in cardiovascular pathology. • Mitophagy and mitochondrial dynamics influence cardiovascular disease progression. • Ferroptosis, cuproptosis, pyroptosis, necroptosis, NETosis, and disulfidptosis crosstalk with mitochondria. • Disrupted mitochondrial quality control exacerbates cardiomyocyte injury. • Targeting these pathways may preserve mitochondrial integrity and cardiac function.

BACKGROUND:Chronic heart failure (CHF) has become a significant global disease burden due to its high prevalence, re-hospitalization rate, and mortality rate. Decreased exercise tolerance is a typical manifestation of CHF patients, which severely impairs their quality of life. Yiqi Fumai injection (YQFM), an injectable drug, is a representative medication recommended by Chinese guidelines for the treatment of CHF. It has significant advantages in improving the clinical symptoms and quality of life of CHF patients. However, there is still a lack of high-quality evidence-based evidence to support clinical decisions in improving exercise tolerance. PURPOSE:The aim of this study was to evaluate the clinical effect of YQFM in improving the exercise tolerance of patients with CHF, and to promote the overall prevention and treatment level of CHF. STUDY DESIGN AND METHODS:This was a single-center, prospective, open-label, randomized, controlled clinical trial that included patients with heart failure (CHF) who had a brain natriuretic peptide (BNP) level > 35 ng/L, NYHA cardiac function classification of grades II to IV, and were aged 18 to 90 years, and were recruited at the First Affiliated Hospital of Tianjin University of Traditional Chinese Medicine from January 2024 to February 2025. The random allocation sequence was generated using the block randomization method to randomly assign the subjects to the control group (conventional Western medicine treatment) or the YQFM group (conventional Western medicine treatment + injection of Yiqi Fumai). The intervention period was 10 days, and the follow-up period was 60 days. The primary outcome measure was the metabolic equivalent (METs) predicted by the Veterans Specific Activity Questionnaire (VSAQ). Secondary outcome measures included 6-minute walk distance (6MWD), NYHA cardiac function classification, BNP level, cardiac ultrasound indicators, and the Kansas City Cardiomyopathy Patient Quality of Life Scale (KCCQ) score. Safety assessments of adverse events and laboratory indicators were conducted throughout the trial period. The outcome indicators were analyzed using the complete analysis set, following the intention-to-treat (ITT) principle. RESULTS:A total of 204 CHF patients completed this study. The intention-to-treat analysis showed that compared with the control group, the YQFM group had significantly higher METs at 10 days of treatment, 30 days of follow-up, and 60 days of follow-up (P < 0.05), and the improvement in METs at 60 days of follow-up was more significant [4.91 ± 1.02 vs 4.53 ± 0.96; Mean difference: 0.38; 95% CI: 0.11-0.65; P = 0.006]. The YQFM group also had significantly higher 6MWD at 10 days of treatment, 30 days of follow-up, and 60 days of follow-up compared with the control group (P < 0.05), and the improvement in 6MWD at 60 days of follow-up was more significant [347.0 (288.5, 403.3) vs 308.0 (278.0, 365.0); Median difference: 27.00; 95% CI: 8.00-49.00; P = 0.006]. The NYHA cardiac function classification, serum BNP concentration, LVEF, KCCQ score, etc. all showed significant improvement at 10 days of treatment, 30 days of follow-up, and 60 days of follow-up compared with the control group. In addition, no increased risk of adverse events was observed when using YQFM. CONCLUSIONS:YQFM has remarkable efficacy in enhancing the exercise tolerance and quality of life of patients with CHF, as well as improving their cardiac function. It also has good safety profiles.

Heart failure (HF) represents a serious manifestation or advanced stage of various cardiac diseases. HF continues to impose a significant global disease burden, characterized by high rates of hospitalization and fatality. Furthermore, the pathogenesis and pathophysiological processes underlying HF remain incompletely understood, complicating its prevention and treatment strategies. One significant pathophysiological mechanism associated with HF is the systemic inflammatory response. PANoptosis, a novel mode of inflammatory cell death, has been extensively studied in the context of infectious diseases, neurodegenerative disorders, cancers, and other inflammatory conditions. Recent investigations have revealed that PANoptosis-related genes are markedly dysregulated in HF specimens. Consequently, the PANoptosis-mediated inflammatory response may represent a potential mechanism and therapeutic target for HF. This paper conducts a comprehensive analysis of the molecular pathways that drive PANoptosis. We discuss its role and potential therapeutic targets in HF, thereby providing valuable insights for clinical treatment and the development of novel therapies.

The continuous development of antitumor therapy has significantly reduced the mortality of patients with malignancies. However, the antitumor-related cardiotoxicity has become the leading cause of long-term mortality in patients with malignancies. Besides, the pathogenesis of antitumor-related cardiotoxicity is still unclear, and practical means of prevention and treatment are lacking in clinical practice. Therefore, the major challenge is how to combat the cardiotoxicity of antitumor therapy effectively. More and more studies have shown that antitumor therapy kills tumor cells while causing damage to sensitive tissues such as the intestinal mucosa, leading to the increased permeability of the intestine and the dysbiosis of intestinal microecology. In addition, the dysbiosis of intestinal microecology contributes to the development and progression of cardiovascular diseases through multiple pathways. Thus, the dysbiosis of intestinal microecology may be a potential mechanism and target for antitumor-related cardiotoxicity. We summarized the characteristics of intestinal microecology disorders induced by antitumor therapy and the association between intestinal microecological dysbiosis and CVD. And on this basis, we hypothesized the potential mechanisms of intestinal microecology mediating the occurrence of antitumor-related cardiotoxicity. Then we reviewed the previous studies targeting intestinal microecology against antitumor-associated cardiotoxicity, aiming to provide a reference for future studies on the occurrence and prevention of antitumor-related cardiotoxicity by intestinal microecology.

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As the population ages, the prevalence of age-related frailty increases sharply, which increases the risk of poor health status of older adults, such as disability, falls, hospitalization, and death. Across the globe, frailty is moving toward the forefront of health and medical research. Currently, frailty is believed to be preventable and reversible, so the early identification of frailty is critical. However, there are neither precise biomarkers of frailty nor definitive laboratory tests and corresponding clinical testing techniques and equipment in clinical practice. As a result, the clinical identification of frailty is mainly achieved through the widely used frailty scale, which is an objective, simple, time-saving, effective, economical, and feasible measurement tool. In this narrative review, we summarized and analyzed the various existing frailty scales from different perspectives of screening and evaluation, aiming to provide a reference for clinical researchers and practitioners to judge and manage frail older people accurately.

Frailty syndrome denotes a decreased capacity of the body to maintain the homeostasis and stress of the internal environment, which simultaneously increases the risk of adverse health outcomes in older adults, including disability, hospitalization, falls, and death. To promote healthy aging, we should find strategies to cope with frailty. However, the pathogenesis of frailty syndrome is not yet clear. Recent studies have shown that the diversity, composition, and metabolites of gut microbiota significantly changed in older adults with frailty. In addition, several frailty symptoms were alleviated by adjusting gut microbiota with prebiotics, probiotics, and symbiosis. Therefore, we attempt to explore the pathogenesis of frailty syndrome in older people from gut microbiota and summarize the existing interventions for frailty syndrome targeting gut microbiota, with the aim of providing timely and necessary interventions and assistance for older adults with frailty.

CONTEXT:Autophagy-apoptosis is the core mechanism of doxorubicin-induced myocardial injury. miR-30a is a pivotal factor in the regulation of autophagy and apoptosis. It remains unclear whether SMI exerts cardioprotective effect by regulating autophagy and apoptosis via miR-30a.OBJECTIVE:This study evaluates the effects of SMI on ameliorating doxorubicin-induced myocardial injury.MATERIALS AND METHODS:The level of LDH and CK, and the expression of miR-30a was detected. mCherry-EGFP-LC3B double fluorescence was used to observe autophagy flow. Apoptosis was detected by Annexin V/PI staining. Western Blot was used to estimate the expression of autophagy related proteins and apoptosis-related proteins.RESULTS:Compared with the control group, there were evidently decreased cell viability, elevated level of LDH and CK, down-regulated expression of miR-30a in the model group. Data from Western blot and fluorescence indicated that doxorubicin contributed to the elevated autophagy and apoptosis. Compared with the model group, there were increased cell viability, decreased level of LDH and CK, and up-regulated expression of miR-30a in the Shenmai group and the Shenmai + miR-30a inhibitor group. Meanwhile, the results manifested that there were suppressed autophagy flow accompanied by the down-regulated expression of Beclin-1, LC3-II, LC3-II/LC3-I and up-regulated expression of p62 protein, and declined apoptosis rate accompanied by the up-regulated Bcl2 expression and the down-regulated expression of Bax, Cleaved Caspase-9, Cleaved Caspase-9/Caspase-9, Cleaved Caspase-3, Cleaved Caspase-3/Caspase-3 in the Shenmai group and the Shenmai + miR-30a inhibitor group.DISCUSSION AND CONCLUSION:Shenmai injection inhibited autophagy and apoptosis via miR-30a, thereby alleviating doxorubicin-induced myocardial injury.

基于文献梳理防治抗肿瘤药物心脏毒性的中药注射液,主要为生脉注射液、参麦注射液、参附注射液、参芪扶正注射液、康艾注射液、黄芪注射液、心脉隆注射液、丹红注射液、丹参注射液、红花注射液、复方苦参注射液、华蟾素注射液、银杏达莫注射液等,其效应机制主要有抗氧化应激、抑制细胞凋亡、减轻炎症反应等,为中医药防治抗肿瘤药物心脏毒性提供依据.

Heart Failure (HF) has been one of the leading causes of death worldwide. Though its latent mechanism and therapeutic manipulation are updated and developed ceaselessly, there remain great gaps in the cognition of heart failure. High morbidity and readmission rates among HF patients are waiting to be addressed. Recent studies have found that myocardial energy metabolism was closely related to heart failure, in which substrate utilization, as well as intermediate metabolism disorders, insulin resistance, oxidative stress, and mitochondrial dysfunction, might underlie systolic dysfunction and progression of HF. This article centers on the changes and counteraction of cardiac energy metabolism in the failing heart. Therefore, targeting impaired energy provision is of great potential in the treatment of HF. And shifting the objective from traditional neurohormones to improving the cellular environment is expected to further optimize the management of HF.

目的:分析蒽环类药物心脏毒性患者的临床特征及中医证候分布.方法:纳入2017年9月至2019年12月于天津中医药大学第一附属医院及新疆医科大学附属中医医院住院的蒽环类药物心脏毒性患者104例,采集并分析患者的相关信息,运用系统聚类分析患者的临床特征和证候特点.结果:共纳入蒽环类药物心脏毒性患者104例,其症状见心悸(96.15％)、乏力(76.92％)、面色淡白(74.04％)、气短(45.19％)等;舌脉以舌淡(61.54％)或舌淡胖(36.54％),苔白(44.23％)或苔少(41.35％),脉弦(27.88％)或脉弱(25.00％)为主;常见中医症状可聚为6类,辨证为阴虚火旺证、心阳不振证、气阴两虚证、心血亏虚证、脾虚湿困证、胆郁痰扰证.结论:蒽环类药物心脏毒性患者以心悸、乏力、面色淡白、气短为核心症状,证候分型以阴虚火旺证、心阳不振证、气阴两虚证、心血亏虚证、脾虚湿困证、胆郁痰扰证为主.

OBJECTIVE:To systematically evaluate the efficacy of Shengmai San in patients with cardiotoxicity of anthracyclines. METHODS:Randomized controlled trials (RCTs) were identified by searching China National Knowledge Infrastructure (CNKI), Wanfang Database, Chinese Biomedical Literature Database (CBM), PubMed, Cochrane Library, and Embase Databases from the inceptions until December 2020. The Cochrane Handbook was used to evaluate the risk of bias in the included studies. Data analysis was conducted using RevMan 5.3 software. RESULTS:Totally 19 RCTs with 2,331 participants were included in this review. Results showed that in improving arrhythmia (13 RCTs, n=1,877, RR=0.37, 95%CI 0.25 to 0.52, P<0.00001), the treatment group was superior to the control group. In terms of reducing left ventricular end-diastolic diameter (LVEDD, 2 RCTs, n=128, MD=-0.79, 95%CI -0.93 to -0.65, P<0.00001) and left ventricular end systolic diameter (LVESD, 2 RCTs, n=128, MD=-0.58, 95%CI -0.82 to -0.35, P<0.00001), the treatment group was also better than the control group. In reducing myocardial enzymes such as creatine kinase (CK) [(3 RCTs, n=256, SMD=-0.80, 95%CI -1.16 to -0.44, P<0.0001), (2 RCTs, n=126, SMD=-0.62, 95%CI -0.98 to -0.26, P=0.0007)], the treatment group was superior to the control group. CONCLUSION:Shengmai San has a positive effect on the treatment of cardiotoxicity from anthracyclines. However, in the future, it is still necessary to conduct high-quality RCTs to verify its efficacy.