Cardiovascular aging: from cellular and molecular changes to therapeutic interventions

Figures

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  Figure 1.. Cellular processes and signaling pathways that are common in myocardial and vascular aging. Oxidative stress and mitochondrial dysfunction in the aged cardiovascular system are associated with decreased SIRT1 levels, which increases p66Shc and Arg2 levels, as well as the expression of NOX4, while it decreases Klotho levels, resulting in higher NRF2 proteolysis. Aging decreases AMPK activation in the cardiovascular system, leading to increased mTORC1 activity, increases ROCK1 and ROCK2, and decreases Parkin, resulting in impaired autophagy. Assembly of NLRP3 inflammasome, and elevated expression of TLR4 and NF-κΒ in the aged heart and arteries result in higher production of inflammatory cytokines, while the increased levels of Ang II, ROCK1 and ROCK2, and the decreased levels of PAR2 are associated with age-related cardiac and arterial fibrosis; image created on biorender.com.

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  Figure 2.. Interventions in preclinical studies that have translated into improvements in cardiac and/or vascular aging in humans (overlapping area) include exercise, caloric restriction, caloric restriction mimetics, such as spermidine, and SGLT2-inhibitors; image created on biorender.com.