Results 21 to 30 of about 75,749 (306)

Mitophagy coordinates the mitochondrial unfolded protein response to attenuate inflammation-mediated myocardial injury

open access: yesRedox Biology, 2021
Mitochondrial dysfunction is a fundamental challenge in septic cardiomyopathy. Mitophagy and the mitochondrial unfolded protein response (UPRmt) are the predominant stress-responsive and protective mechanisms involved in repairing damaged mitochondria ...
Yue Wang   +5 more
doaj   +1 more source

Mitophagy for cardioprotection

open access: yesBasic Research in Cardiology, 2023
AbstractMitochondrial function is maintained by several strictly coordinated mechanisms, collectively termed mitochondrial quality control mechanisms, including fusion and fission, degradation, and biogenesis. As the primary source of energy in cardiomyocytes, mitochondria are the central organelle for maintaining cardiac function.
Allen Sam Titus   +3 more
openaire   +2 more sources

MitoQ inhibits hepatic stellate cell activation and liver fibrosis by enhancing PINK1/parkin-mediated mitophagy

open access: yesOpen Medicine, 2021
Mitophagy affects the activation of hepatic stellate cells (HSCs). Mitochondria-targeted ubiquinone (MitoQ) is a mitochondria-targeted antioxidant that reduces the production of intracellular reactive oxygen species (ROS).
Dou Shi-Ying   +7 more
doaj   +1 more source

Chemical mitophagy modulators: Drug development strategies and novel regulatory mechanisms

open access: yesPharmacological Research, 2023
Maintaining mitochondrial homeostasis is a potential therapeutic strategy for various diseases, including neurodegenerative diseases, cardiovascular diseases, metabolic disorders, and cancer. Selective degradation of mitochondria by autophagy (mitophagy)
Yu Dong   +10 more
doaj   +1 more source

AMBRA1 is able to induce mitophagy via LC3 binding, regardless of PARKIN and p62/SQSTM1 [PDF]

open access: yes, 2014
Damaged mitochondria are eliminated by mitophagy, a selective form of autophagy whose dysfunction associates with neurodegenerative diseases. PINK1, PARKIN and p62/SQTMS1 have been shown to regulate mitophagy, leaving hitherto ill-defined the ...
A Follenzi   +46 more
core   +7 more sources

Mitophagy in ototoxicity

open access: yesFrontiers in Cellular Neuroscience, 2023
Mitochondrial dysfunction is associated with ototoxicity, which is caused by external factors. Mitophagy plays a key role in maintaining mitochondrial homeostasis and function and is regulated by a series of key mitophagy regulatory proteins and signaling pathways.
Hezhou Han   +7 more
openaire   +3 more sources

Mitophagy Regulation Following Myocardial Infarction

open access: yesCells, 2022
Mitophagy, which mediates the selective elimination of dysfunctional mitochondria, is essential for cardiac homeostasis. Mitophagy is regulated mainly by PTEN-induced putative kinase protein-1 (PINK1)/parkin pathway but also by FUN14 domain-containing 1 (
Annie Turkieh   +3 more
doaj   +1 more source

A Mammalian Mitophagy Receptor, Bcl2-L-13, Recruits the ULK1 Complex to Induce Mitophagy

open access: yesCell Reports, 2019
Summary: Degradation of mitochondria by selective autophagy, termed mitophagy, contributes to the control of mitochondrial quality. Bcl2-L-13 is a mammalian homolog of Atg32, which is an essential mitophagy receptor in yeast.
Tomokazu Murakawa   +5 more
doaj   +1 more source

Mitophagy and cancer [PDF]

open access: yesCancer & Metabolism, 2015
Mitophagy is a selective form of macro-autophagy in which mitochondria are selectively targeted for degradation in autophagolysosomes. Mitophagy can have the beneficial effect of eliminating old and/or damaged mitochondria, thus maintaining the integrity of the mitochondrial pool.
Chourasia, Aparajita H   +2 more
openaire   +2 more sources

Baicalein Activates Parkin-Dependent Mitophagy through NDP52 and OPTN

open access: yesCells, 2022
The elimination of intracellular components by autophagy maintains metabolic homeostasis and is a quality-control pathway that enables organelle regeneration.
Po-Yuan Ke   +2 more
doaj   +1 more source

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