聚焦衰老的心脏：对射血分数保留型心力衰竭的深入了解

IF 12.5 1区医学 Q1 CELL BIOLOGY

Ageing Research Reviews Pub Date : 2024-10-12 DOI:10.1016/j.arr.2024.102542

Zhewei Zhang , Yu Wang , Xiangqi Chen , Chuan Wu , Jingyue Zhou , Yan Chen , Xiaojing Liu , Xiaoqiang Tang

{"title":"聚焦衰老的心脏：对射血分数保留型心力衰竭的深入了解","authors":"Zhewei Zhang , Yu Wang , Xiangqi Chen , Chuan Wu , Jingyue Zhou , Yan Chen , Xiaojing Liu , Xiaoqiang Tang","doi":"10.1016/j.arr.2024.102542","DOIUrl":null,"url":null,"abstract":"<div><div>Heart failure with preserved ejection fraction (HFpEF) accounts for 50 % of heart failure (HF) cases, making it the most common type of HF, and its prevalence continues to increase in the aging society. HFpEF is a systemic syndrome resulting from many risk factors, such as aging, metabolic syndrome, and hypertension, and its clinical features are highly heterogeneous in different populations. HFpEF syndrome involves the dysfunction of multiple organs, including the heart, lung, muscle, and vascular system. The heart shows dysfunction of various cells, including cardiomyocytes, endothelial cells, fibroblasts, adipocytes, and immune cells. The complex etiology and pathobiology limit experimental research on HFpEF in animal models, delaying a comprehensive understanding of the mechanisms and making treatment difficult. Recently, many scientists and cardiologists have attempted to improve the clinical outcomes of HFpEF. Recent advances in clinically related animal models and systemic pathology studies have improved our understanding of HFpEF, and clinical trials involving sodium-glucose cotransporter 2 inhibitors have significantly enhanced our confidence in treating HFpEF. This review provides an updated comprehensive discussion of the etiology and pathobiology, molecular and cellular mechanisms, preclinical animal models, and therapeutic trials in animals and patients to enhance our understanding of HFpEF and improve clinical outcomes.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"101 ","pages":"Article 102542"},"PeriodicalIF":12.5000,"publicationDate":"2024-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The aging heart in focus: The advanced understanding of heart failure with preserved ejection fraction\",\"authors\":\"Zhewei Zhang , Yu Wang , Xiangqi Chen , Chuan Wu , Jingyue Zhou , Yan Chen , Xiaojing Liu , Xiaoqiang Tang\",\"doi\":\"10.1016/j.arr.2024.102542\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Heart failure with preserved ejection fraction (HFpEF) accounts for 50 % of heart failure (HF) cases, making it the most common type of HF, and its prevalence continues to increase in the aging society. HFpEF is a systemic syndrome resulting from many risk factors, such as aging, metabolic syndrome, and hypertension, and its clinical features are highly heterogeneous in different populations. HFpEF syndrome involves the dysfunction of multiple organs, including the heart, lung, muscle, and vascular system. The heart shows dysfunction of various cells, including cardiomyocytes, endothelial cells, fibroblasts, adipocytes, and immune cells. The complex etiology and pathobiology limit experimental research on HFpEF in animal models, delaying a comprehensive understanding of the mechanisms and making treatment difficult. Recently, many scientists and cardiologists have attempted to improve the clinical outcomes of HFpEF. Recent advances in clinically related animal models and systemic pathology studies have improved our understanding of HFpEF, and clinical trials involving sodium-glucose cotransporter 2 inhibitors have significantly enhanced our confidence in treating HFpEF. This review provides an updated comprehensive discussion of the etiology and pathobiology, molecular and cellular mechanisms, preclinical animal models, and therapeutic trials in animals and patients to enhance our understanding of HFpEF and improve clinical outcomes.</div></div>\",\"PeriodicalId\":55545,\"journal\":{\"name\":\"Ageing Research Reviews\",\"volume\":\"101 \",\"pages\":\"Article 102542\"},\"PeriodicalIF\":12.5000,\"publicationDate\":\"2024-10-12\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Ageing Research Reviews\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S156816372400360X\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CELL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Ageing Research Reviews","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S156816372400360X","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CELL BIOLOGY","Score":null,"Total":0}

引用次数: 0

摘要

射血分数保留型心力衰竭（HFpEF）占心力衰竭（HF）病例的 50%，是最常见的心力衰竭类型，随着老龄化社会的到来，其发病率持续上升。HFpEF 是一种由多种风险因素（如衰老、代谢综合征和高血压）导致的全身性综合征，其临床特征在不同人群中具有高度异质性。HFpEF 综合征涉及多个器官的功能障碍，包括心脏、肺、肌肉和血管系统。心脏中的心肌细胞、内皮细胞、成纤维细胞、脂肪细胞和免疫细胞等多种细胞均出现功能障碍。复杂的病因和病理生物学限制了对高频心衰动物模型的实验研究，延迟了对其机制的全面了解，给治疗带来困难。最近，许多科学家和心脏病专家都在尝试改善 HFpEF 的临床疗效。与临床相关的动物模型和系统病理学研究的最新进展提高了我们对 HFpEF 的认识，而钠-葡萄糖共转运体 2 抑制剂的临床试验则大大增强了我们治疗 HFpEF 的信心。本综述对病因和病理生物学、分子和细胞机制、临床前动物模型以及动物和患者治疗试验进行了最新的全面讨论，以加深我们对 HFpEF 的理解并改善临床疗效。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

查看原文本刊更多论文

The aging heart in focus: The advanced understanding of heart failure with preserved ejection fraction

Heart failure with preserved ejection fraction (HFpEF) accounts for 50 % of heart failure (HF) cases, making it the most common type of HF, and its prevalence continues to increase in the aging society. HFpEF is a systemic syndrome resulting from many risk factors, such as aging, metabolic syndrome, and hypertension, and its clinical features are highly heterogeneous in different populations. HFpEF syndrome involves the dysfunction of multiple organs, including the heart, lung, muscle, and vascular system. The heart shows dysfunction of various cells, including cardiomyocytes, endothelial cells, fibroblasts, adipocytes, and immune cells. The complex etiology and pathobiology limit experimental research on HFpEF in animal models, delaying a comprehensive understanding of the mechanisms and making treatment difficult. Recently, many scientists and cardiologists have attempted to improve the clinical outcomes of HFpEF. Recent advances in clinically related animal models and systemic pathology studies have improved our understanding of HFpEF, and clinical trials involving sodium-glucose cotransporter 2 inhibitors have significantly enhanced our confidence in treating HFpEF. This review provides an updated comprehensive discussion of the etiology and pathobiology, molecular and cellular mechanisms, preclinical animal models, and therapeutic trials in animals and patients to enhance our understanding of HFpEF and improve clinical outcomes.

求助全文

通过发布文献求助，成功后即可免费获取论文全文。去求助

来源期刊

Ageing Research Reviews 医学-老年医学

CiteScore

19.80

自引率

2.30%

发文量

216

审稿时长

55 days

期刊介绍： With the rise in average human life expectancy, the impact of ageing and age-related diseases on our society has become increasingly significant. Ageing research is now a focal point for numerous laboratories, encompassing leaders in genetics, molecular and cellular biology, biochemistry, and behavior. Ageing Research Reviews (ARR) serves as a cornerstone in this field, addressing emerging trends. ARR aims to fill a substantial gap by providing critical reviews and viewpoints on evolving discoveries concerning the mechanisms of ageing and age-related diseases. The rapid progress in understanding the mechanisms controlling cellular proliferation, differentiation, and survival is unveiling new insights into the regulation of ageing. From telomerase to stem cells, and from energy to oxyradical metabolism, we are witnessing an exciting era in the multidisciplinary field of ageing research. The journal explores the cellular and molecular foundations of interventions that extend lifespan, such as caloric restriction. It identifies the underpinnings of manipulations that extend lifespan, shedding light on novel approaches for preventing age-related diseases. ARR publishes articles on focused topics selected from the expansive field of ageing research, with a particular emphasis on the cellular and molecular mechanisms of the aging process. This includes age-related diseases like cancer, cardiovascular disease, diabetes, and neurodegenerative disorders. The journal also covers applications of basic ageing research to lifespan extension and disease prevention, offering a comprehensive platform for advancing our understanding of this critical field.