Mechanisms of mitophagy

By R. Youle, Derek P. Narendra. Nature reviews. Molecular cell biology, 2011

3,203 citations recorded by the source corpus.

Autophagy not only recycles intracellular components to compensate for nutrient deprivation but also selectively eliminates organelles to regulate their number and maintain quality control. Mitophagy, the specific autophagic elimination of mitochondria, has been identified in yeast, mediated by autophagy-related 32 (Atg32), and in mammals during red blood cell differentiation, mediated by NIP3-like protein X (NIX; also known as BNIP3L). Moreover, mitophagy is regulated in many metazoan cell types by parkin and PTEN-induced putative kinase protein 1 (PINK1), and mutations in the genes encoding these proteins have been linked to forms of Parkinson's disease.

Subfields: Epidemiology, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/104e16d31bdcb9691d4d2bc22232e30b2f5a328f

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Citations in the corpus

Autophagy‐based unconventional secretory pathway for extracellular delivery of IL‐1β (2011, background): “…cellular viability (Kroemer and Levine, 2008; Kroemer et al, 2010) by removing damaged organelles, for example, depolarized or leaky mitochondria (Youle and Narendra, 2011), digesting potentially toxic protein aggregates (Renna et al, 2010), killing intracellular microbes (Deretic and Levine,…”
A new pathway for mitochondrial quality control: mitochondrial‐derived vesicles (2014, background): “Mitophagy is an important mechanism to remove entirely dysfunctional mitochondria, whether linked to global protein misfolding or depolarization (Youle & Narendra, 2011).”
Landscape of the PARKIN-dependent ubiquitylome in response to mitochondrial depolarization (2013, background): “Potential PARKIN-regulated functions include: (1) fission–fusion cycles (FIS1, TBC1D15), (2) small molecule transport (VDACs), (3) apoptosis (FKBP8, MCL1, BAX), (4)”
The Roles of PINK1, Parkin and Mitochondrial Fidelity in Parkinson's Disease (2015, background): “…that loss of mitochondrial membrane potential (DJm), known to prevent protein import into mitochondria through the TIM complex, which in turn prevents PINK1 proteolysis, was the unifyingmechanism through which diverse mitochondrial stresses induced PINK1 accumulation (Youle and Narendra, 2011).”
Interactions between autophagy receptors and ubiquitin-like proteins form the molecular basis for selective autophagy. (2014, background): “Mitophagy-Specific Receptors In response to severe damage, mitochondria are degraded by autophagy (Figure 1) (reviewed in Youle and Narendra, 2011).”
ER stress: Autophagy induction, inhibition and selection (2015, background): “It is also evident that selective autophagy peaks during development, pathogenic infections, and alteration of nutrient sources.(169) Interestingly, selective autophagy was first described in yeast, which is mainly based on the autophagy-like process called the cytoplasm to vacuole targeting (Cvt) p”
Mechanisms of Selective Autophagy (2016, neutral): “Another intriguing possibility is that during selective autophagy, the presence of the cargo induces the formation of isolation membranes [65,97,98].”
Cellular mitophagy: Mechanism, roles in diseases and small molecule pharmacological regulation (2023, background): “to the identification of two proteins (PINK1 and Parkin) connected to the familial form of PD, the process of mitophagy, which is essential for maintaining neuronal homeostasis, is frequently associated with PD [57].”
Extracellular M. tuberculosis DNA Targets Bacteria for Autophagy by Activating the Host DNA-Sensing Pathway (2012, positive): “In contrast, selective autophagy functions to specifically renovate the cell by targeting protein aggregates and specific organelles for removal through the use of ubiquitin-mediated targeting (Youle and Narendra, 2011).”
Mitochondrial dynamics and mitochondrial quality control (2014, background): “This is an open access article under the CC BY-NC-SA license (http://creativecommons.org/licenses/by-nc-sa/3.0/).”