Trends in Biochemical Sciences
SpotlightSpecial Issue: Mitochondria & MetabolismMitochondrial Dysfunction Meets Senescence
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2022, Anti-Aging PharmacologyLung aging and senescence in health and disease
2022, Cellular Senescence in DiseaseLipidomics reveals carnitine palmitoyltransferase 1C protects cancer cells from lipotoxicity and senescence
2021, Journal of Pharmaceutical AnalysisCitation Excerpt :A collective review of recent studies has proven that the main mechanism of senescence is lipid peroxidation and oxidative stress [12,13]. Excess lipids are vulnerable to the attack by reactive oxygen species (ROS) and conversion into toxic reactive lipid peroxides and oxidized lipids (oxi-lipid), which could have lipotoxic effects on mitochondrial DNA (mtDNA), RNA and proteins of mitochondrial machinery, and oxidation equilibrium, further leading to mitochondrial dysfunction and senescence [8,14,15]. In addition, it was reported that senescence could be a physiological degenerative process accelerated by lipotoxic insults, while conversely, the process of senescence can make cells more vulnerable to lipotoxicity [16].
Mechanistic insights into AMPK-SIRT3 positive feedback loop-mediated chondrocyte mitochondrial quality control in osteoarthritis pathogenesis
2021, Pharmacological ResearchCitation Excerpt :This organelle not only plays a dominating role in oxidative phosphorylation (OXPHOS) and central carbon metabolism but is also closely related to a variety of biological processes that determine cell fate [31]. When the mitochondrial structure or function is damaged, a series of cellular and histopathological changes are induced due to the excessive accumulation of reactive oxygen species (ROS), the release of pro-apoptotic factors, and activation of the immune system, among other stimuli [31,32]. Recent reports on the connections between mitochondrial function and aging biology have emerged.
MFN2 contributes to metabolic disorders and inflammation in the aging of rat chondrocytes and osteoarthritis
2020, Osteoarthritis and CartilageCitation Excerpt :Similar phenomenon also occurs in hypertrophic chondrocytes, that hypertrophic chondrocytes rely more on mitochondrial respiration specifically in hypertrophic zone of the growth plate, as well as in OA cartilage25,26. Further, no significant differences in cellular senescence related changes were found, as we demonstrated that mitochondrial dysfunction contributed to metabolic disorders above all, it would not be unreasonable to assume that age-related mitochondrial dysfunction was prior to cellular senescence and might contribute to normal aging as well as OA27,28. Mitochondrial fission and fusion contribute to changes in mitochondrial morphology and cell metabolism29.