Mitofusin 2 Participates in Mitophagy and Mitochondrial Fusion Against Angiotensin II-Induced Cardiomyocyte Injury

Conclusion: Mitofusin 2 promotes Parkin translocation and phosphorylation, leading to mitophagy to clear damaged mitochondria. However, the beneficial effects of MFN2 were reversed by autophagy inhibitors. Additionally, MFN2 participates in mitochondrial fusion to maintain mitochondrial quality. Thus, MFN2 participated in mitophagy and mitochondrial fusion against Ang II-induced cardiomyocyte injury. Introduction Ventricular remodeling is the core foundation for the development of heart failure (Hill and Olson, 2008). Pathological remodeling is typically due to a number of causes that result in increased pressure or volume, causing pressure or volume overload in the heart (Burchfield et al., 2013). This pathological process may include ventricular hypertrophy, ventricular dilation, cardiomegaly, and other changes. Ultimately, ventricular remodeling results in heart failure. Neurohumoral stimulation and mechanical stress are the major triggers of ventricular remodeling. Ang II can activate a number of signaling pathways to induce cardiac inflammation, hypertrophy, and fibrosis, thus leading to ventricular remodeling (Mehta and Griendling, 2007; Trachtenberg and Hare, 2017). Additionally, ventricular remodeling involves mitochondrial metabolism, oxidative stress, and autophagy (Maillet et al., 2013; van Berlo et al., 2013; Zhou et al., 2013; Lyon et al., 2015). In recent years, insufficient myocardial energy has been considered one of the mechanisms underlying the occu...
Source: Frontiers in Physiology - Category: Physiology Source Type: research