The role of epicardial adipose tissue remodelling in heart failure with preserved ejection fraction

被引：3

作者：

Janssen-Telders, Carolina ^{[1
,2
]}

Eringa, Etto C. ^{[2
,3
,4
]}

de Groot, Joris R. ^{[1
,2
]}

de Man, Frances S. ^{[2
,4
]}

Handoko, M. Louis ^{[1
,5
,6
]}

机构：

[1] Amsterdam UMC, Heart Ctr, Dept Cardiol, Boelelaan 1117, NL-1081 HV Amsterdam, Netherlands

[2] Amsterdam Cardiovasc Sci, Boelelaan 1108, NL-1081 HZ Amsterdam, Netherlands

[3] Amsterdam UMC, Dept Physiol, Boelelaan 1117, NL-1081 HV Amsterdam, Netherlands

[4] Maastricht UMC, Cardiovasc Res Inst Maastricht, Dept Physiol, Univ Singel 50, NL-6229 ER Maastricht, Netherlands

[5] Amsterdam UMC, Dept Pulmonol, Boelelaan 1117, NL-1081 HV Amsterdam, Netherlands

[6] Univ Med Ctr Utrecht, Dept Cardiol, Heidelberglaan 100, NL-3584 CX Utrecht, Netherlands

来源：

CARDIOVASCULAR RESEARCH | 2025年 / 121卷 / 06期

关键词：

Heart failure with preserved ejection fraction; Epicardial adipose tissue; Inflammation; Inflammatory pathways; BINDING-PROTEIN; 4; CORONARY-ARTERY-DISEASE; INSULIN-RESISTANCE; BARIATRIC SURGERY; POTENTIAL ROLE; ACTIVIN-A; IN-VIVO; FAT; ADIPONECTIN; OBESITY;

D O I：

10.1093/cvr/cvaf056

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Heart failure with preserved ejection fraction (HFpEF) is a growing global health problem characterized by high morbidity and mortality, with limited effective therapies available. Obesity significantly influences haemodynamic and structural changes in the myocardium and vasculature, primarily through the accumulation and action of visceral adipose tissue. Particularly, epicardial adipose tissue (EAT) contributes to HFpEF through inflammation and lipotoxic infiltration of the myocardium. However, the precise signalling pathways leading to diastolic stiffness in HFpEF require further elucidation. This review explores the dynamic role of EAT in health and disease. Drawing upon insights from studies in other conditions, we discuss potential EAT-mediated inflammatory pathways in HFpEF and how they may contribute to functional and structural myocardial and endothelial derangements, including intramyocardial lipid infiltration, fibrosis, endothelial dysfunction, cardiomyocyte stiffening, and left ventricular hypertrophy. Lastly, we propose potential targets for novel therapeutic avenues.

引用

页码：860 / 870

页数：11

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