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Review
. 2020 Jul 1;319(1):C166-C182.
doi: 10.1152/ajpcell.00021.2020. Epub 2020 May 20.

Cardiac tissue remodeling in healthy aging: the road to pathology

Evan Tracy  1 , Gabrielle Rowe  1 , Amanda J LeBlanc  1
Affiliations
Review

Cardiac tissue remodeling in healthy aging: the road to pathology

Evan Tracy et al. Am J Physiol Cell Physiol. .

Abstract

This review aims to highlight the normal physiological remodeling that occurs in healthy aging hearts, including changes that occur in contractility, conduction, valve function, large and small coronary vessels, and the extracellular matrix. These "normal" age-related changes serve as the foundation that supports decreased plasticity and limited ability for tissue remodeling during pathophysiological states such as myocardial ischemia and heart failure. This review will identify populations at greater risk for poor tissue remodeling in advanced age along with present and future therapeutic strategies that may ameliorate dysfunctional tissue remodeling in aging hearts.

Keywords: aging; cardiac; remodeling.

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Conflict of interest statement

No conflicts of interest, financial or otherwise, are declared by the authors.

Figures

Fig. 1.
Fig. 1.
Cardiac tissue remodeling with advancing age. The effect of advancing age and senescence on remodeling of the coronary vasculature (A and E), heart valves (B), conduction system (C), cardiac mechanical properties as assessed via echocardiography (D), and cardiomyoctyes and extracellular matrix (F) are shown. ACE-1, angiotensin-converting enzyme-1; ECM, extracellular matrix; HF, heart failure; HIF-1, hypoxia-inducing factor-1; Ito, transient outward potassium channel; IVRT, isovolumic relaxation time; LTCC, L-type calcium channel; LV, left ventricle; MMP-2, matrix metalloproteinase-2; NO, nitric oxide; PDGF, platelet-derived growth factor; ROS, reactive oxygen species; VEGF, vascular endothelial growth factor.
Fig. 2.
Fig. 2.
Age-dependent inflammatory and fibrotic response to myocardial infarction (MI) as a consequence of tissue remodeling in aging. Inflammatory and fibrotic profiles of young heart tissue at baseline and postmyocardial infarction (A) compared with aged heart tissue at baseline and post-MI (D). Cross section of heart, with healthy tissue in red; young hearts form a stable scar (solid gray) (B), while aged hearts form a weak loose scar (nonsolid and thin) (E). Histology of scar collagen network using Sirius Red-stained section of young (C) and senescent (F) mouse infarct. CRP, C-reactive protein; DHEAS, dehydroepiandrosterone sulfate; MCP-1, monocyte chemoattractant protein-1.
See this image and copyright information in PMC

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