Mitochondrial Quality Control in Aging and Heart Failure: Influence of Ketone Bodies and Mitofusin-Stabilizing Peptides
Conclusion: We conclude that elevated KB levels were beneficial for mitochondrial repair in the aging heart. However, an impaired MFN2-DRP1-mediated fusion-fission process in HF reduced this benefit, as well as Parkin degradation and mitophagic signaling cascade.
Introduction
The incidence of cardiovascular disease, including heart failure (HF), has increased steadily in the United States as the general population has aged (Roger et al., 2004; Savarese and Lund, 2017). Mitochondria are essential for energy generation to maintain cardiac contraction during each heartbeat. However, mitochondrial function declines during aging and HF, leading to accumulation of depolarized mitochondria and a decline in ATP production, thereby resulting in impaired ability of the heart to pump blood (Wallace, 2005; Lopez-Otin et al., 2013; Abdellatif et al., 2018). To counteract these adverse effects, cells are able to monitor, mark, and effectively remove damaged mitochondria through a selective mitochondrial macro-autophagy, or mitophagy (Kim et al., 2007; Hammerling and Gustafsson, 2014; Kotiadis et al., 2014; Linton et al., 2015).
Effective degradation and removal of dysfunctional mitochondria is extremely important for cardiac myocyte survival (Linton et al., 2015). Mitochondrial membrane depolarization activates serine/threonine kinase PTEN-inducible kinase 1 (PINK1, encoded by PARK6) accumulation on the mitochondrial su...
Source: Frontiers in Physiology - Category: Physiology Source Type: research
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