The DOI matches its Crossref record; 67 of the 67 references it cites were found in a registry or an index.
Molecular mechanisms and physiological functions of mitophagy
Open accessAbstract
Degradation of mitochondria via a selective form of autophagy, named mitophagy, is a fundamental mechanism conserved from yeast to humans that regulates mitochondrial quality and quantity control. Mitophagy is promoted via specific mitochondrial outer membrane receptors, or ubiquitin molecules conjugated to proteins on the mitochondrial surface leading to the formation of autophagosomes surrounding mitochondria. Mitophagy-mediated elimination of mitochondria plays an important role in many processes including early embryonic development, cell differentiation, inflammation, and apoptosis. Recent advances in analyzing mitophagy in vivo also reveal high rates of steady-state mitochondrial turnover in diverse cell types, highlighting the intracellular housekeeping role of mitophagy. Defects in mitophagy are associated with various pathological conditions such as neurodegeneration, heart failure, cancer, and aging, further underscoring the biological relevance. Here, we review our current molecular understanding of mitophagy, and its physiological implications, and discuss how multiple mitophagy pathways coordinately modulate mitochondrial fitness and populations.
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2 retracted
Mitochondrial Autophagy Is an HIF-1-dependent Adaptive Metabolic Response to Hypoxia
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RetractedRETRACTED ARTICLE: Parkin and PINK1 mitigate STING-induced inflammation
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RetractedLC3, a mammalian homologue of yeast Apg8p, is localized in autophagosome membranes after processing.
Kabeya, Y., Mizushima, N., Ueno, T., Yamamoto, A., Kirisako, T., Noda, T., Kominami, E., Ohsumi, Y., & Yoshimori, T. (2000) · The EMBO Journal · doi:10.1093/emboj/19.21.5720 · Cited by 6,605
Global burden of NAFLD and NASH: trends, predictions, risk factors and prevention
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Querfurth, H. W., & LaFerla, F. M. (2010) · New England Journal of Medicine · doi:10.1056/nejmra0909142 · Cited by 4,569
Parkin is recruited selectively to impaired mitochondria and promotes their autophagy
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Hereditary Early-Onset Parkinson's Disease Caused by Mutations in PINK1
Valente, E. M., Abou-Sleiman, P. M., Caputo, V., Muqit, M. M. K., Harvey, K., Gispert, S., Ali, Z., Del Turco, D., Bentivoglio, A. R., Healy, D. G., et al. (2004) · Science · doi:10.1126/science.1096284 · Cited by 3,481
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PINK1 Is Selectively Stabilized on Impaired Mitochondria to Activate Parkin
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PINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1
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Cited by
Mitochondria at the crossroads of health and disease
Suomalainen, A., & Nunnari, J. (2024) · Cell · doi:10.1016/j.cell.2024.04.037 · Cited by 478
ROS: Basic Concepts, Sources, Cellular Signaling, and its Implications in Aging Pathways
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Mechanisms of Selective Autophagy
Lamark, T., & Johansen, T. (2021) · Annual Review of Cell and Developmental Biology · doi:10.1146/annurev-cellbio-120219-035530 · Cited by 429
Mitochondrial dysfunction in aging
Guo, Y., Guan, T., Shafiq, K., Yu, Q., Jiao, X., Na, D., Li, M., Zhang, G., & Kong, J. (2023) · Ageing Research Reviews · doi:10.1016/j.arr.2023.101955 · Cited by 339
Mitochondria-associated programmed cell death as a therapeutic target for age-related disease
Nguyen, T. T., Wei, S., Nguyen, T. H., Jo, Y., Zhang, Y., Park, W., Gariani, K., Oh, C.-M., Kim, H. H., Ha, K.-T., et al. (2023) · Experimental & Molecular Medicine · doi:10.1038/s12276-023-01046-5 · Cited by 325
Metadata
- Authors
- Onishi, M., Yamano, K., Sato, M., Matsuda, N., & Okamoto, K.
- Venue
- The EMBO Journal
- Published
- 2021-01-13
- Volume
- 40
- Issue
- 3
- Pages
- e104705-e104705
- ISSN
- 0261-4189 (ISSN-L)
- 1460-2075
- OpenAlex
- W3121008513
- Cited by
- 1,416
- References
- 67
- FWCI
- 130.67
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Onishi, M., Yamano, K., Sato, M., Matsuda, N., & Okamoto, K. (2021). Molecular mechanisms and physiological functions of mitophagy. The EMBO Journal. https://doi.org/10.15252/embj.2020104705
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.