![]() ![]() For example, defects in proteostasis have been alleviated in longevity models utilizing overexpression of mitochondrial‐targeted catalase, 19, 20, 21, 22 calorie restriction (CR), 23 reduced IGF1 signaling, 18, 24, 25 and rapamycin (RM) treatment. While dysfunction of protein quality control mechanisms is a hallmark of aging, improvement of these mechanisms is associated with longevity and health. Interventions that extend healthspan and lifespan in various animal models have also suggested an important role of protein homeostasis in health and aging. 11, 12 The importance of proteostasis is illustrated by many studies indicating that age‐related diseases and conditions are associated with the inability of the cell to maintain healthy proteins or eliminate defective proteins, 13 as observed in neurodegenerative diseases, 14 cardiac dysfunction, 15, 16 cataracts, 17 and sarcopenia. Loss of proteostasis is a “hallmark” of aging 1, 2 that manifests at the cellular level in a number of ways, such as protein aggregation, 3 unfolding, 4 oxidative damage, 5, 6 post‐translational modification, 7, 8, 9, 10 and altered rates of protein turnover. The ability to maintain and fine‐tune this equilibrium in response to internal and external cues is essential for cellular and organismal health. Protein homeostasis (proteostasis) is the maintenance of a functional equilibrium between protein synthesis, fidelity, folding, localization, modification, and degradation. ![]()
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