fig1

Molecular mechanisms underlying sarcopenia in heart failure

Figure 1. Molecular mechanisms linking heart failure (HF) and sarcopenia. HF patients have reduced exercise tolerance, malnutrition, and altered hormonal signaling, including changes to aldosterone, angiotensin, cortisol, and catecholamine levels, all of which are linked to muscle wasting. Both HF and sarcopenia are associated with mitochondrial changes, including loss of maximal energy production and altered fuel utilization, increased oxidative stress, changes to mitochondrial fission/fusion leading to structural abnormalities, mitochondrial DNA (mtDNA) damage, and reduced mitochondrial protein quality control. Both HF and sarcopenia also have altered protein production and turnover, most notably involving autophagy and the ubiquitin-protease system (UPS), leading to proteostatic stress. Finally, HF is associated with chronic inflammation, particularly as evidenced by increased cytokine signaling involving TNF-α, IL-1, and IL-6, leading to muscle loss.

The Journal of Cardiovascular Aging

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