Normal functioning of mitochondria is crucial for cardiac performance. Mitochondria undergo mitophagy (mitochondrial autophagy) and biogenesis, and mitochondrial proteins are subject to extensive post-translational modifications (PTMs). The state of mitochondrial homeostasis reflects overall cellular fitness and longevity. Perturbed mitochondria produce less adenosine triphosphate (ATP), release greater amounts of reactive molecules, and are more prone to apoptosis. Therefore mitochondrial turnover is an integral aspect of quality control in which dysfunctional mitochondria are selectively eliminated through mitophagy. Currently, the progressive deterioration of physiological functions is seen as accumulation of modified/damaged proteins with limiting regenerative ability throughout aging in myocardial cells. Mitochondrial stress response to reactive species was evaluated as electron transport chain (ETC) complexes, redox-active molecules, and their possible communication. Protein-protein interactions revealed a strong linkage between age and ETC protein subunits. Redox state was strongly affected in senescent mitochondria with shift in favor of more pro-oxidizing condition within cardiomyocytes. Assume all together, dysfunctional proteostasis can play a causative role in aging and restoration of protein homeostasis machinery is protective against aging and possibly age-related disorders.
Part of the book: Mitochondrial Diseases