IntroductionAtrial fibrillation (AF) is the most common and clinically significant arrhythmia requiring treatment. Although an imbalance between the sympathetic and vagal branches of autonomic nervous system (ANS) is known to trigger and sustain AF, the underlying mechanisms remain incompletely understood. Furthermore, there are yet no clinically authorized antiarrhythmic drugs currently targeting the modulation of ANS.MethodsTargeted LC–MS/MS profiling of plasma 39 neurotransmitters was conducted in a clinical cohort. To identify shared mechanisms, atrial transcriptomes and a sympathetic neuron activation dataset were integrated with DEGs, WGCNA, enrichment, immune infiltration, and machine-learning feature selection, and in silico docking was performed. For in vivo validation, an Ang II–infused mouse model with valsartan intervention was utilized, including transesophageal burst pacing, immunostaining, immunoblotting, and efferocytosis quantification.ResultsPlasma from AF patients exhibited an autonomic-imbalance signature (upregulated monoaminergic and downregulated cholinergic neurotransmitters). Shared ANS–AF bioinformatic analysis highlighted hub genes as CDKN2D, FYTTD1, LRR1, and POPDC3. Immune analyses pinpointed CD47-mediated efferocytosis as a crucial link. In vivo, Ang II induced autonomic remodeling, Ca²⁺-handling suppression, increased apoptosis with CD47/SIRPα upregulation, impaired efferocytosis, and heightened inflammatory signaling; valsartan partially reversed these changes.DiscussionMulti-omics and in vivo evidence suggests an ANS–immune–atrial remodeling axis in which CD47–SIRPα–dependent efferocytosis blockade is highly associated with atrial inflammation and AF susceptibility, with valsartan acting as a clinically relevant modulator of this pathway.

BackgroundPyroptotic signaling involving nuclear factor-kappa B (NF-κB) and NOD-like receptor family pyrin domain–containing 3 (NLRP3) has been implicated in chronic heart failure (CHF). Xin-Fu-Kang (XFK) is a nine-herb formula used clinically for CHF with “qi deficiency and blood stasis.” Although cardioprotective effects have been reported, it remains unclear whether XFK modulates myocardial pyroptotic signaling via miR-223–dependent regulation of NF-κB.MethodsA CHF model was established by permanent left anterior descending coronary artery (LADCA) ligation in rats, and an in vitro oxygen–glucose deprivation/reoxygenation (OGD/R) injury model was generated in H9c2 cardiomyocytes. Cardiac structure and function were assessed by transthoracic echocardiography and histology. Myocardial inflammation and pyroptotic signaling were quantified by ELISA for interleukin-1 beta (IL-1β) and interleukin-18 (IL-18), and by immunoblotting for NLRP3, pro-caspase-1/caspase-1 ratio, Apoptosis-associated speck-like protein containing a CARD (ASC), cleaved gasdermin D N-terminal fragment (GSDMD-N), and NF-κB p65 phosphorylation. Nuclear–cytoplasmic fractionation and immunofluorescence tracked p65 translocation. Causality was probed by miR-223 gain- and loss-of-function, with functional rescue using a miR-223 inhibitor. RT-qPCR was used to measure the mRNA levels of NF-κB p65 and miR-223.ResultsLADCA produced marked systolic dysfunction with chamber dilation, increased myocardial IL-1β and IL-18, increased NLRP3, ASC, GSDMD-N, and p65 phosphorylation, and decreased the pro-caspase-1/caspase-1 ratio. XFK improved cardiac function and structural integrity, attenuated fibrosis and cardiomyocyte apoptosis, reduced inflammatory cytokines, and diminished NLRP3 and ASC abundance. In OGD/R-injured H9c2 cells, XFK preserved viability, limited lactate dehydrogenase release, decreased NLRP3, ASC, GSDMD-N, and IL-1β, increased the pro-caspase-1/caspase-1 ratio, and restrained NF-κB activation by reducing p65 phosphorylation and nuclear translocation. Mechanistically, XFK upregulated miR-223, and miR-223 overexpression reproduced the suppression of pyroptosis-related readouts linked to NF-κB/NLRP3 signaling. Inhibition of miR-223 attenuated the protective effects of XFK, supporting the interpretation that XFK-mediated modulation of NF-κB-related inflammatory signaling is at least partly dependent on miR-223.ConclusionNF-κB–linked NLRP3 pyroptotic signaling represents a prominent feature in the CHF model examined. These findings suggest that XFK exerts protective effects in CHF via miR-223–dependent modulation of NF-κB/NLRP3 pyroptotic signaling, supporting its potential adjunctive strategy to mitigate inflammation-driven cardiac dysfunction.

Background: Chronic heart failure (CHF) is the terminus of a variety of cardiovascular diseases. Xin-Fu-Kang oral liquid (XFK), a natural herbal compound, has been used in CHF treatment for decades. However, further investigation is required to elucidate the fundamental mechanisms. Study Design and Methods: Transverse aortic constriction (TAC) was performed in mouse models. The pharmacological efficacy of XFK was confirmed by assessing cardiac function and the observation of pathological alterations in myocardial tissue. Following this, single-cell sequencing (scRNA-seq) was implemented. With the identification of XFK metabolites in rat serum via UPLC-QE MS, molecular docking was utilized to conduct preliminary validation of putative therapeutic targets. Subsequently, the phenylephrine-induced model of cardiac pressure overload was established for conducting additional verification and rescue experiments by silencing NR4A1 in vitro. Results: XFK intervention significantly ameliorated cardiac function in the TAC-induced CHF model. Based on scRNA-seq, cardiomyocytes exhibited the most notable alterations following XFK intervention, with NR4A1 identified as a significantly differentially expressed gene after both TAC induction and XFK intervention. In vitro experiments demonstrated that XFK enhanced mitochondrial function, mitigated oxidative stress, and restored mitophagy in a NR4A1-dependent manner, consequently decreasing apoptosis in PE-induced H9C2. Furthermore, the upstream mechanism was associated with capacity of XFK to mitigate endoplasmic reticulum stress and regulate crosstalk between the two organelles. Conclusion: XFK counteracts cardiac chronic pressure overload through regulating NR4A1-mediated functional interaction between endoplasmic reticulum and mitochondria in cardiomyocytes, further preserves mitochondria function and prevents apoptosis. This finding indicates a novel pharmacological therapy for CHF.

Background:Autophagy is essential for the homeostasis and function of the cardiovascular system. Citespace is a visual analysis software developed in the context of scientometrics and data visualization. The purpose of this study is to use Citespace software to conduct bibliometric and visual analysis of the research on autophagy in cardiovascular diseases, identify the current status, hot spots and trends in this field, help researchers clarify the future research focus and direction of autophagy in cardiovascular diseases, and provide more positive and broader ideas for the treatment and drug development of cardiovascular diseases.Methods:In the Web of Science Core Collection database to download the data from 2004 to 2022 regarding autophagy in cardiovascular research. CitespaceV was used to collect the research status, hotspots and development trends for visual analysis.Results:The 3568 articles were published by 547 authors from 397 institutions in 75 countries. From 2004 to 2021, the annual publications increased over time. The top 3 productive nations were China, the United States, and Germany. The leading institution was China's Fudan University. The most cited paper is Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition). The research hotpots include monitoring methods for autophagy activity, changes in autophagy levels in different types of cardiovascular diseases, autophagy signal transduction mechanism in cardiovascular diseases, etc.Conclusion:Bibliometric analysis provided valuable information for autophagy research in cardiovascular disease, which is full of opportunities and challenges. The research of autophagy in the field of cardiovascular diseases is still worthy of in-depth exploration. A challenge with autophagy-targeted therapies is their dichotomy in which the goal is to target maladaptive autophagy while maintaining a baseline level of cell survival to optimize a beneficial outcome. It is necessary for scientists to develop new methods to evaluate the level of autophagy from basic application to human body and reveal the signaling mechanism of autophagy in different types of cardiovascular diseases.

Cardiac remodeling is a shared pathological change in most cardiovascular diseases. Encompassing both adaptive physiological responses and decompensated pathological changes. Anatomically, atrial remodeling is primarily caused by atrial fibrillation, whereas ventricular remodeling is typically induced by myocardial infarction, hypertension, or cardiomyopathy. Mitochondria, the powerhouse of cardiomyocytes, collaborate with other organelles such as the endoplasmic reticulum to control a variety of pathophysiological processes such as calcium signaling, lipid transfer, mitochondrial dynamics, biogenesis, and mitophagy. This mechanism is proven to be essential for cardiac remodeling. Post-translational modifications can regulate intracellular signaling pathways, gene expression, and cellular stress responses in cardiac cells by modulating protein function, stability, and interactions, consequently shaping the myocardial response to injury and stress. These modifications, in particular phosphorylation, acetylation, and ubiquitination, are essential for the regulation of the complex molecular pathways that underlie cardiac remodeling. This review provides a comprehensive overview of the crosstalk between the endoplasmic reticulum and mitochondria during cardiac remodeling, focusing on the regulatory effects of various post-translational modifications on these interactions.

Background: Tanshinone IIA, derived from Radix Salviae Miltiorrhizae (Salvia miltiorrhiza Bunge), constitutes a significant component of this traditional Chinese medicine. Numerous studies have reported positive outcomes regarding its influence on cardiac function. However, a comprehensive comprehension of the intricate mechanisms responsible for its cardioprotective effects is still lacking. Methods: A rat model of heart failure (HF) induced by acute myocardial infarction (AMI) was established via ligation of the left anterior descending coronary artery. Rats received oral administration of tanshinone IIA (1.5 mg/kg) and captopril (10 mg/kg) for 8 weeks. Cardiac function was assessed through various evaluations. Histological changes in myocardial tissue were observed using staining techniques, including Hematoxylin and Eosin (HE), Masson, and transmission electron microscopy. Tunel staining was used to detect cell apoptosis. Serum levels of NT-pro-BNP, IL-1β, and IL-18 were quantified using enzyme-linked immunosorbent assay (ELISA). Expression levels of TLR4, NF-κB p65, and pyroptosis-related proteins were determined via western blotting (WB). H9C2 cardiomyocytes underwent hypoxia-reoxygenation (H/R) to simulate ischemia-reperfusion (I/R) injury, and cell viability and apoptosis were assessed post treatment with different tanshinone IIA concentrations (0.05 μg/ml, 0.1 μg/ml). ELISA measured IL-1β, IL-18, and LDH expression in the cell supernatant, while WB analysis evaluated TLR4, NF-κB p65, and pyroptosis-related protein levels. NF-κB p65 protein nuclear translocation was observed using laser confocal microscopy. Results: Tanshinone IIA treatment exhibited enhanced cardiac function, mitigated histological cardiac tissue damage, lowered serum levels of NT-pro-BNP, IL-1β, and IL-18, and suppressed myocardial cell apoptosis. Moreover, tanshinone IIA downregulated the expression of TLR4, NF-κB p65, IL-1β, pro-IL-1β, NLRP3, Caspase-1, and GSDMD-N pyroptosis-related proteins in myocardial tissue. Additionally, it bolstered H/R H9C2 cardiomyocyte viability, curbed cardiomyocyte apoptosis, and reduced the levels of TLR4, NF-κB p65, IL-1β, pro-IL-1β, NLRP3, Caspase-1, and GSDMD-N pyroptosis-related proteins in H/R H9C2 cells. Furthermore, it hindered NF-κB p65 protein nuclear translocation. Conclusion: These findings indicate that tanshinone IIA enhances cardiac function and alleviates myocardial injury in HF rats following AMI. Moreover, tanshinone IIA demonstrates potential suppression of cardiomyocyte pyroptosis. These effects likely arise from the inhibition of the TLR4/NF-κB p65 signaling pathway, presenting a promising therapeutic target.

目的 研究RhoA/ROCK信号通路及相关炎症因子核转录因子κBp65(NF-κBp65)、细胞间黏附分子-1(ICAM-1)、基质金属蛋白酶抑制因子1(TIMP-1)在原发性高血压病中的表达及与原发性高血压病的相关性.方法 选取广安门医院于2020年8月至2020年12月收治的120例原发性高血压病患者为观察组,并同期纳入本院体检的30例无高血压病的健康人群为对照组.比较两组间静脉血Rho相关卷曲螺旋形成蛋白激酶2(ROCKⅡ)、NF-κBp65、TIMP-1、ICAM-1表达水平及静脉血单核细胞中RhoAmRNA、ROCKⅡmRNA表达水平,探究其与原发性高血压病的相关性,并以原发性高血压病的危险因素及通路相关指标ROCKⅡ、NF-κBp65、ICAM-1、TIMP-1和RhoAmRNA、ROCKⅡmRNA为自变量,以是否患有原发性高血压病为因变量进行二元Logistic回归分析,绘制ROC曲线分析RhoA/ROCK通路调控的炎性因子对原发性高血压病的预测效力.结果 与对照组相比,观察组ROCKⅡ、NF-κBp65、ICAM-1、TIMP-1、RhoAmRNA、ROCKⅡmRNA表达水平均有不同程度升高(P<0.05).二元Logistic回归分析显示,ROCKⅡmRNA(OR=3.698,95％CI:1.365～10.014,P<0.05)、ROCKⅡ(OR=1.143,95％CI:1.068～1.223,P<0.001)、NF-κBp65(OR=1.486,95％CI:1.106～1.997,P<0.01)与原发性高血压病密切相关.对ROCKⅡmRNA、ROCKⅡNF-κBp65绘制与疾病相关的ROC曲线,评估参数预测效力,曲线下面积分别为ROCKⅡmRNA:0.791(95％CI:0.714～0.869,P<0.001);ROCKⅡ:0.887(95％CI:0.823～0.95,P<0.001);NF-κBp65:0.807(95％CI:0.731～0.884,P<0.001).结论 原发性高血压病病变程度与RhoAmRNA、ROCKⅡmRNA、ROCKⅡ、NF-κBp65、TIMP-1、ICAM-1变化幅度均呈正相关.并与ROCKⅡmRNA、ROCKⅡNF-κBp65密切相关.提示原发性高血压病的发生发展与RhoA/ROCKⅡ通路有密切联系.

Background One of the most prominent features of living organisms is their circadian rhythm, which governs a wide range of physiological processes and plays a critical role in maintaining optimal health and function in response to daily environmental changes. This work applied bibliometric analysis to explore quantitative and qualitative trends in circadian rhythm in cardiovascular diseases (CVD). It also aims to identify research hotspots and provide fresh suggestions for future research. Methods The Web of Science Core Collection was used to search the data on circadian rhythm in CVD. HistCite, CiteSpace, and VOSviewer were used for bibliometric analysis and visualization. The analysis included the overall distribution of yearly outputs, top nations, active institutions and authors, core journals, co-cited references, and keywords. To assess the quality and efficacy of publications, the total global citation score (TGCS) and total local citation score (TLCS) were calculated. Results There were 2102 papers found to be associated with the circadian rhythm in CVD, with the overall number of publications increasing year after year. The United States had the most research citations and was the most prolific country. Hermida RC, Young ME, and Ayala DE were the top three writers. The three most notable journals on the subject were Chronobiology International, Hypertension Research, and Hypertension. In the early years, the major emphasis of circadian rhythm in CVD was hormones. Inflammation, atherosclerosis, and myocardial infarction were the top developing research hotspots. Conclusion Circadian rhythm in CVD has recently received a lot of interest from the medical field. These topics, namely inflammation, atherosclerosis, and myocardial infarction, are critical areas of investigation for understanding the role of circadian rhythm in CVD. Although they may not be future research priorities, they remain of significant importance. In addition, how to implement these chronotherapy theories in clinical practice will depend on additional clinical trials to get sufficient trustworthy clinical evidence.

Rho/ROCK通路与细胞的生长、发育、分化以及迁移密切相关.大量研究表明Rho/ROCK途径与炎症细胞因子的相互作用对糖尿病、眼炎症性疾病、肿瘤、肺损伤、心脏病和神经损伤性疾病的发生发展产生了一定的影响,以该通路作为疾病的治疗靶点越来越得到人们的广泛关注,通过总结近年来Rho/ROCK信号通路与炎症细胞因子的相关研究,为中药降压、抗动脉粥样硬化的进一步研究提供参考.

The mitochondrial unfolded protein response (UPRmt) is a stress response pathway that regulates the expression of mitochondrial chaperones, proteases, and other proteins involved in protein folding and degradation, thereby ensuring proper mitochondrial function. In addition to this critical function, the UPRmt also plays a role in other cellular processes such as mitochondrial biogenesis, energy metabolism, and cellular signaling. Moreover, the UPRmt is strongly associated with various diseases. From 2004 to 2022, there has been a lot of interest in UPRmt. The present study aims to utilized bibliometric tools to assess the genesis, current areas of focus, and research trends pertaining to UPRmt, thereby highlighting avenues for future research. There were 442 papers discovered to be related to UPRmt, with the overall number of publications rising yearly. International Journal of Molecular Sciences was the most prominent journal in this field. 2421 authors from 1,402 institutions in 184 nations published studies on UPRmt. The United States was the most productive country (197 documents). The top three authors were Johan Auwerx, Cole M Haynes, and Dongryeol Ryu. The early focus of UPRmt is "protein." And then the UPRmt research shifted from Caenorhabditis elegans back to mammals, and its close link to aging and various diseases. The top emerging research hotspots are neurodegenerative diseases and metabolic diseases. These findings provide the trends and frontiers in the field of UPRmt, and valuable information for clinicians and scientists to identify new perspectives with potential collaborators and cooperative countries.

目的 运用CiteSpace软件对心血管疾病组学研究进行文献计量可视化分析,探究组学在心血管疾病中的运用现状和研究热点.方法 检索Web of Science Core Collection数据库(WOSCC),将检索到有关心血管疾病组学研究的数据导入CiteSpace绘制知识图谱,对作者、机构、地区、关键词和共被引文献进行可视化分析.结果 心血管疾病组学研究有关文献发文量从2016年起呈爆发上升趋势.发文量靠前的作者有Matthias Schittmayer和Ruth Birnergruenberger等,国家有美国、德国、英国等,机构有哈佛医学院、格拉斯哥大学、华盛顿大学等.关键词分析显示研究热点集中于疾病风险、炎症、死亡率、肠道微生物群的研究.Nikpay M(2015)、Kundaje A(2015)、Wang TJ(2011)的3篇核心共被引文献为该领域研究的基础.结论 通过文献计量学分析,心血管病组学领域目前正处于研究高热期,但作者间合作较少.代谢组学和蛋白质组学运用较广且热度持续.组学应用于心血管疾病研究具有诊断、治疗、预测疾病风险等作用,可发现疾病本质并用于开发新的预防治疗策略.

目的 探讨高血压病人血清唾液酸(SA)与冠心病的相关性.方法 选取原发性高血压病人648例,按照是否患有冠心病,将病人分成冠心病组(501例)与非冠心病组(147例),比较两组间血清SA及各生化指标.结果 两组性别、2型糖尿病占比、年龄、尿素氮(BUN)、血肌酐、血清清蛋白(ALB)、血清球蛋白(GLB)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、总胆红素(TBIL)、间接胆红素(IDBIL)比较,差异均有统计学意义(P<0.05),冠心病组血清SA高于非冠心病组(P<0.05).Spearman相关性分析显示,冠心病的发生与年龄、尿素氮、血肌酐、GLB、SA呈正相关(P<0.05),与ALB、LDL-C、IDBIL呈负相关(P<0.05).多因素Logistic分析显示,年龄、性别、血清SA、IDBIL均是冠心病的影响因素.结论 年龄、性别、血清SA、IDBIL为高血压继发冠心病的影响因素.

The aim of this study was to gain insight into the progress and dynamics of psycho-cardiological disease research and track its hot spots. We have analyzed psycho-cardiological disease-related literature extracted from the Web of Science (WOS) Core Collection from 2001 to 2021 with the help of Cite Space. As a result, we have included 5,032 records. Then, we have analyzed connected networks for the country, author, subject category, keywords, and cited reference. We have summarized the findings in four aspects. First, the annual quantitative distribution of publications is on the rise, although there is a slight drop. Second, in terms of country analysis, the United States, England, Australia, Germany, and Italy are the main research forces in psycho-cardiological diseases. At the same time, several academic entities represented by Andrew Steptoe and Roland von Känel, MD, have been formed based on the early consciousness of physical and mental health in these countries. Besides, China is also more concerned about it due to the rapid population aging process and the largest population. Third, the psycho-cardiological disease is multidisciplinary, including psychology, psychiatry, clinical medicine, such as cardiovascular system and neurology, public environmental and occupational health, and pharmacology. Finally, the results of keyword analysis and co-cited references indicate the hot spots and frontiers in psycho-cardiological disease. The hot spots in psycho-cardiological disease include three aspects. The first aspect includes psychosocial factors, such as depression, lack of social support, and low economic and social status; the second aspect includes priority populations, such as Alzheimer's disease dementia caregivers, elderly, and patients with cancer, and the third aspect includes interventions, such as exercise therapy and diet. In addition, there are three future research frontiers. The first is a psycho-cardiological disease in patients with COVID-19; the second is cardiac rehabilitation, especially exercise therapy and health behavior evaluation; and the final is evidence-based medical evaluation, such as systematic reviews and meta-analyses.

趋化因子已成为各疾病领域研究的热点，通过借助PubMed、UniProtKB数据库归纳和完善了目前已知的趋化因子配体及其对应结合的受体、趋化因子的来源及主要趋化功效等；总结了趋化因子在冠状动脉粥样硬化性心脏病及心房颤动等心血管疾病中的研究进展。得出趋化因子配体或结合相关受体组成一定的信号通路发挥作用，涉及机制多集中在促炎、促纤维化、促动脉粥样硬化等方面。

Takotsubo cardiomyopathy (TTC) is often acute with a high mortality rate and is subject to relapse. Meanwhile, its complex pathogenesis has attracted increasing attention. To learn more about TTC, CiteSpace V.5.7 R5W was used in this study to analyze the research status, hot spots, and trends in TTC before 2020. The keywords, co-citation references, as well as country and institution distribution were explored. A total of 2,349 papers were reviewed. The United States, Italy, and Germany were the main countries studying TTC and had good cooperation relationships. The Mayo Clinic topped the institution list, but the rate of inter-institutional cooperation was not high. Research hotspots include disease features, auxiliary diagnostic methods, epidemiology, and pathophysiological mechanisms, and the latest ones are complications related to prognosis, such as cardiovascular abnormalities caused by myocardial infarction and normal or non-obstructive coronary arteries (MINOCA), atrial fibrillation, stroke, cancer, and COVID-19. In conclusion, the research of TTC is in a hot development period. Our research will help clinicians and researchers to better understand TTC and its research status by providing a foundation for research objectives. In doing this, our research will help to provide better scientific management, diagnosis, and treatment for patients with TTC, which will in turn improve the prognosis of this condition.

目的 运用CiteSpace软件对过氧化物酶体增殖物激活受体(PPAR)与脂代谢相关文献进行可视化分析,发现该领域近年来研究热点、趋势及研究进展.方法 以Web of Science核心合集数据库为研究对象,运用CiteSpace 5.7 R2对文献进行可视化分析,探讨该领域国家、机构发文量,关键热词、高质量被引文献等,并导出相关图谱.结果 共纳入文献8737篇,PPARγ与脂代谢是出现频次最高的关键词,Pawlak M(2015)是被引频次最高的文献,TONTONOZP是被引频次最高的作者,美国是发文量最多的国家.结论 以CiteSpace为工具,对PPAR与脂代谢相关文献进行可视化分析,可提供该领域的研究热点及趋势.

目的 为探索中医药在动脉粥样硬化领域近5年的研究现状、热点及趋势,对相关文献进行计量、共现及可视化分析.方法 检索中国知网数据库2015年1月至2020年1月中医药治疗动脉粥样硬化的相关文献,筛查后将文献导入CiteSpace,分析发文量情况,对作者和机构进行共现分析,对关键词进行共现分析和聚类分析等.结果 2015年以来,中医药在动脉粥样硬化领域的发文量总体呈上升趋势.中医药在动脉粥样硬化领域存在大量分散作者,也存在较为稳定且高产的研究团队.主要研究机构较为分散.热点关键词形成10个聚类.2018—2020年,网络药理学成为热点突现词.结论 中医药在动脉粥样硬化领域的发文量总体呈上升趋势,动脉粥样硬化用药规律、机制及并发症的研究是近年来的研究热点和主要趋势.

Pyroptosis is a kind of programmed cell death closely related to inflammation. The pathways that mediate pyroptosis can be divided into the Caspase-1-dependent canonical pathway and the Caspase4/5/11-dependent non-canonical pathway. The most significant difference from other cell death is that pyroptosis rapidly causes rupture of the plasma membrane, cell expansion, dissolution and rupture of the cell membrane, the release of cell contents and a large number of inflammatory factors, and send pro-inflammatory signals to adjacent cells, recruit inflammatory cells and induce inflammatory responses. Cardiac remodeling is the basic mechanism of heart failure (HF) and the core of pathophysiological research on the underlying mechanism. A large number of studies have shown that pyroptosis can cause cardiac fibrosis, cardiac hypertrophy, cardiomyocytes death, myocardial dysfunction, excessive inflammation, and cardiac remodeling. Therefore, targeting pyroptosis has a good prospect in improving cardiac remodeling in HF. In this review, the basic molecular mechanism of pyroptosis is summarized, the relationship between pyroptosis and cardiac remodeling in HF is analyzed in-depth, and the potential therapy of targeting pyroptosis to improve adverse cardiac remodeling in HF is discussed, providing some ideas for improving the study of adverse cardiac remodeling in HF.

Cardiovascular disease is a group of diseases with high mortality in clinic, including hypertension, coronary heart disease, cardiomyopathy, heart valve disease, heart failure, to name a few. In the development of cardiovascular diseases, pathological cardiac remodeling is the most common cardiac pathological change, which often becomes a domino to accelerate the deterioration of the disease. Therefore, inhibiting pathological cardiac remodeling may delay the occurrence and development of cardiovascular diseases and provide patients with greater long-term benefits. Resveratrol is a non-flavonoid polyphenol compound. It mainly exists in grapes, berries, peanuts and red wine, and has cardiovascular protective effects, such as anti-oxidation, inhibiting inflammatory reaction, antithrombotic, dilating blood vessels, inhibiting apoptosis and delaying atherosclerosis. At present, the research of resveratrol has made rich progress. This review aims to summarize the possible mechanism of resveratrol against pathological cardiac remodeling, in order to provide some help for the in-depth exploration of the mechanism of inhibiting pathological cardiac remodeling and the development and research of drug targets.