Selective Mitochondrial Autophagy, or Mitophagy, as a Targeted Defense Against Oxidative Stress, Mitochondrial Dysfunction, and Aging
By J. Lemasters. Rejuvenation Research, 2005
1,303 citations recorded by the source corpus.
Subfields: Cell Biology, Epidemiology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/58849130f5b10debd4fef4bafce0f41a9b0d7302
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In Cell Biology
In Epidemiology
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- Koji Yamano
- J. Tschopp
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- Mônica A Delgado
In Molecular Biology
Citations in the corpus
- Cellular mitophagy: Mechanism, roles in diseases and small molecule pharmacological regulation (2023, background): “Within a few years after the word "mitophagy" was initially proposed [6], substantial developments in this field made it possible to identify crucial proteins that specifically mediate mitochondrial breakdown in yeast [7] and”
- Mitophagy: mechanisms, pathophysiological roles, and analysis (2012, background): “Although the exact mechanisms by which autophagy may delay aging are not clear, it has been suggested that mitophagy may help reduce the production of mitochondria-derived ROS and remove dysfunctional mitochondria that would generate mtDNA mutations during aging (Lemasters , 2005 ).”
- The mitophagy pathway and its implications in human diseases (2023, background): “Lemasters first proposed mitophagy in 2005, and pointed out that mitochondrial damage is the signal to initiate mitophagy.(10) Parkinson protein 2 (Parkin) was recruited to mitochondrial depolarization when induced by mitochondrial damage to promote autophagic degradation of mitochondria.”
- Mitochondrial outer-membrane protein FUNDC1 mediates hypoxia-induced mitophagy in mammalian cells (2012, methodology): “(c) HeLa cells were transfected with (Flag)N-Fundc1(1-155)-C(Myc) or (Flag)N-Fundc1(1-139)C(Myc) vectors, respectively.”
- The inflammasome: an integrated view (2011, background): “To protect the cell from the damaging effects of excessive ROS, ROS-generating mitochondria are continuously removed by a form of autophagy termed mitophagy (110).”
- Toll‐like receptors control autophagy (2008, background): “…issue are complicated by the inherent diversity of autophagic targets, represented by a variety of macromolecules, protein aggregates and an assortment of organelles, including mitochondria (Lemasters, 2005), peroxisomes (Farre and Subramani, 2004) and endoplasmic reticulum (Bernales et al, 2006).”
- Molecular mechanisms and physiological functions of mitophagy (2021, positive): “The term “mitophagy” was first coined in 2005 (Lemasters, 2005; Priault et al, 2005), and within a few years, major breakthroughs led to the discovery of key proteins that selectively mediate mitochondrial degradation in yeast (Okamoto et al, 2009; Kanki et al, 2009b) and mammalian cells (Schweers e”
- Oxidative modifications to cellular components in plants. (2007, background): “Another possible strategy has been proposed for mammalian cells where a small, biochemically relatively inactive subpopulation of “breeding” mitochondria in each cell is dividing while the biochemically active, and therefore relatively damaged, mitochondria do not divide (57).”