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Mitochondria in Cell Senescence: Is Mitophagy the Weakest Link?

2017; Elsevier BV; Volume: 21; Linguagem: Inglês

10.1016/j.ebiom.2017.03.020

2352-3964

Viktor I. Korolchuk, Satomi Miwa, Bernadette Carroll, Thomas von Zglinicki,

Advanced Glycation End Products research

Cell senescence is increasingly recognized as a major contributor to the loss of health and fitness associated with aging. Senescent cells accumulate dysfunctional mitochondria; oxidative phosphorylation efficiency is decreased and reactive oxygen species production is increased. In this review we will discuss how the turnover of mitochondria (a term referred to as mitophagy) is perturbed in senescence contributing to mitochondrial accumulation and Senescence-Associated Mitochondrial Dysfunction (SAMD). We will further explore the subsequent cellular consequences; in particular SAMD appears to be necessary for at least part of the specific Senescence-Associated Secretory Phenotype (SASP) and may be responsible for tissue-level metabolic dysfunction that is associated with aging and obesity. Understanding the complex interplay between these major senescence-associated phenotypes will help to select and improve interventions that prolong healthy life in humans.