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Abstract
Mitochondria in the cell are the center for energy production, essential biomolecule synthesis, and cell fate determination. Moreover, the mitochondrial functional versatility enables cells to adapt to the changes in cellular environment and various stresses. In the process of discharging its cellular duties, mitochondria face multiple types of challenges, such as oxidative stress, protein-related challenges (import, folding, and degradation) and mitochondrial DNA damage. They mitigate all these challenges with robust quality control mechanisms which include antioxidant defenses, proteostasis systems (chaperones and proteases) and mitochondrial biogenesis. Failure of these quality control mechanisms leaves mitochondria as terminally damaged, which then have to be promptly cleared from the cells before they become a threat to cell survival. Such damaged mitochondria are degraded by a selective form of autophagy called mitophagy. Rigorous research in the field has identified multiple types of mitophagy processes based on targeting signals on damaged or superfluous mitochondria. In this review, we provide an in-depth overview of mammalian mitophagy and its importance in human health and diseases. We also attempted to highlight the future area of investigation in the field of mitophagy.
Highlights
Mitochondria in the cell are double-membraned organelles, which hold a central role in energy production [1], essential biomolecule synthesis [2], calcium buffering [3] and importantly, in pro-survival or pro-apoptotic signaling [4]
Due to the functional importance of mitochondria, any disturbance in this proteome will leave a profound impact on cell fate and could result in diseases ranging from neurodegenerative disorders and heart diseases to diabetes and cancer [6,7,8,9,10,11]
seven in absentia homolog 1 (SIAH1) at mitochondria polyubiquitinates MOMP, which leads to recruitment of autophagosomes to mitochondria via the autophagy receptor, and LC3 for mitophagy. (MOMP: mitochondrial outer membrane protein) (C) MUL1 based mitophagy: The mitochondrial E3 ubiquitin ligase 1 (MUL1) induces ubiquitin-dependent but PARKIN-independent mitophagy by multiple proposed mechanisms, which are poorly understood and lack consensus
Summary
Mitochondria in the cell are double-membraned organelles, which hold a central role in energy production [1], essential biomolecule synthesis [2], calcium buffering [3] and importantly, in pro-survival or pro-apoptotic signaling [4] These functions are carried out by over 1200 proteins [5], the exact composition of mitochondrial proteins can vary greatly depending on the cell stage, type and environment [5]. The second potential threat to mitochondrial health arises from mitochondrial plasticity, which demands a constant change in the mitochondrial proteome to adapt to cellular needs [16,17] Under such fluctuating conditions, the mitochondrial proteostasis is maintained by a robust mitochondrial import system collaborating with mitochondrial proteases and chaperones [5,16,18,19,20]. PARKIN independent but ubiquitin dependent mitophagy: Ubiquitin-independent or receptor based mitophagy
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