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心脏衰老的免疫机制。

Immune mechanisms of cardiac aging.

作者信息

Goldstein Daniel R, Abdel-Latif Ahmed

机构信息

Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.

Department of Microbiology and Immunology, University of Michigan, Ann Arbor, MI 48109, USA.

出版信息

J Cardiovasc Aging. 2023;3(2). doi: 10.20517/jca.2023.02. Epub 2023 Mar 9.

DOI:10.20517/jca.2023.02
PMID:37092016
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10121185/
Abstract

Advances in healthcare and improvements in living conditions have led to rising life expectancy worldwide. Aging is associated with excessive oxidative stress, a chronic inflammatory state, and limited tissue healing, all of which result in an increased risk of heart failure. In fact, the prevalence of heart failure approaches 40% in the ninth decade of life, with the majority of these cases suffering from heart failure with preserved ejection fraction (HFpEF). In cardiomyocytes (CMs), age-related mitochondrial dysfunction results in disrupted calcium signaling and covalent protein-linked aggregates, which cause cardiomyocyte functional disturbances, resulting in increased stiffness and diastolic dysfunction. Importantly, aging is also associated with chronic low-grade, sterile inflammation, which alters the function of interstitial cardiac cells and leads to cardiac fibrosis. Taken together, cardiac aging is associated with cellular, structural, and functional changes in the heart that contribute to the rising prevalence of heart failure in older people.

摘要

医疗保健的进步和生活条件的改善导致全球预期寿命延长。衰老与过度的氧化应激、慢性炎症状态以及有限的组织修复有关,所有这些都会增加心力衰竭的风险。事实上,在九十岁时心力衰竭的患病率接近40%,其中大多数病例为射血分数保留的心力衰竭(HFpEF)。在心肌细胞(CMs)中,与年龄相关的线粒体功能障碍会导致钙信号传导中断和共价蛋白连接的聚集体,从而引起心肌细胞功能紊乱,导致硬度增加和舒张功能障碍。重要的是,衰老还与慢性低度无菌炎症有关,这种炎症会改变心脏间质细胞的功能并导致心脏纤维化。综上所述,心脏衰老与心脏的细胞、结构和功能变化有关,这些变化导致老年人心力衰竭的患病率不断上升。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6935/10121185/aef3142bae62/nihms-1881770-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6935/10121185/7fe996d86fa5/nihms-1881770-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6935/10121185/aef3142bae62/nihms-1881770-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6935/10121185/7fe996d86fa5/nihms-1881770-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6935/10121185/aef3142bae62/nihms-1881770-f0003.jpg

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