Ageing Research Reviews, Journal Year: 2017, Volume and Issue: 40, P. 64 - 74
Published: Sept. 19, 2017
Language: Английский
Ageing Research Reviews, Journal Year: 2017, Volume and Issue: 40, P. 64 - 74
Published: Sept. 19, 2017
Language: Английский
International Journal of Molecular Sciences, Journal Year: 2021, Volume and Issue: 22(15), P. 8179 - 8179
Published: July 30, 2021
The maintenance of mitochondrial integrity is critical for muscle health. Mitochondria, indeed, play vital roles in a wide range cellular processes, including energy supply, Ca2+ homeostasis, retrograde signaling, cell death, and many others. All mitochondria-containing cells, skeletal dispose several pathways to maintain health, biogenesis, mitochondrial-derived vesicles, dynamics (fusion fission process shaping morphology), mitophagy-the charge the removal mitochondria though autophagy. loss mass (atrophy) major health problem worldwide, especially older people. Currently, there no treatment counteract progressive decline strength that occurs with aging, termed sarcopenia. There increasing data, our own, suggesting accumulation dysfunctional contributes development Impairments mitophagy were recently proposed contribute This review summarizes current state knowledge on role played by We also highlight recent studies showing enhancing promising therapeutic target prevent or even treat dysfunction elderly.
Language: Английский
Citations
175Nature Communications, Journal Year: 2019, Volume and Issue: 10(1)
Published: Feb. 19, 2019
Abstract Autophagy, an evolutionarily conserved cytoplasmic degradation system, has been implicated as a convergent mechanism in various longevity pathways. Autophagic activity decreases with age several organisms, but the underlying is unclear. Here, we show that expression of Rubicon, negative regulator autophagy, increases aged worm, fly and mouse tissues at transcript and/or protein levels, suggesting age-dependent increase Rubicon impairs autophagy over time, thereby curtails animal healthspan. Consistent this idea, knockdown extends worm lifespan ameliorates age-associated phenotypes. Tissue-specific experiments reveal neurons greatest effect on lifespan. knockout mice exhibits reductions interstitial fibrosis kidney reduced α-synuclein accumulation brain. suppressed long-lived worms calorie restricted mice. Taken together, our results suggest suppression autophagic by one signatures aging.
Language: Английский
Citations
170Ageing Research Reviews, Journal Year: 2019, Volume and Issue: 54, P. 100940 - 100940
Published: Aug. 12, 2019
Genetic and pharmacological intervention studies have identified evolutionarily conserved functionally interconnected networks of cellular energy homeostasis, nutrient-sensing, genome damage response signaling pathways, as prominent regulators longevity health span in various species. Mitochondria are the primary sites ATP production key players several other important processes. Mitochondrial dysfunction diminishes tissue organ functional performance is a commonly considered feature aging process. Here we review evidence that through reciprocal multilevel interactions, mitochondria implicated lifespan modulation function these which altogether constitute highly dynamic complex system controls An characteristic pathways their extensive crosstalk apparent malleability to modification by non-invasive pharmacological, dietary, lifestyle interventions, with promising effects on animal models potentially also humans.
Language: Английский
Citations
170Trends in Molecular Medicine, Journal Year: 2022, Volume and Issue: 28(10), P. 836 - 849
Published: July 22, 2022
Language: Английский
Citations
126Antioxidants, Journal Year: 2021, Volume and Issue: 10(5), P. 794 - 794
Published: May 17, 2021
Mitochondrial dysfunction is a hallmark of aging. Dysfunctional mitochondria are recognized and degraded by selective type macroautophagy, named mitophagy. One the main factors contributing to aging oxidative stress, one early responses excessive reactive oxygen species (ROS) production induction mitophagy remove damaged mitochondria. However, mitochondrial damage caused at least in part chronic stress can accumulate, autophagic mitophagic pathways become overwhelmed. The imbalance delicate equilibrium among mitophagy, ROS start, drive, or accelerate process, either physiological aging, pathological age-related conditions, such as Alzheimer’s Parkinson’s diseases. It remains be determined which prime mover this imbalance, i.e., whether it that initiates dysregulation thus activating vicious circle leads reduced ability mitochondria, an alteration regulation leading
Language: Английский
Citations
117Nature Metabolism, Journal Year: 2022, Volume and Issue: 4(7), P. 802 - 812
Published: July 11, 2022
Language: Английский
Citations
117Frontiers in Endocrinology, Journal Year: 2023, Volume and Issue: 14
Published: Jan. 30, 2023
Mitochondria are important organelles that provide cellular energy and play a vital role in cell differentiation apoptosis. Osteoporosis is chronic metabolic bone disease mainly caused by an imbalance osteoblast osteoclast activity. Under physiological conditions, mitochondria regulate the balance between osteogenesis activity maintain homeostasis. pathological mitochondrial dysfunction alters this balance; disruption pathogenesis of osteoporosis. Because osteoporosis, function can be targeted therapeutically osteoporosis-related diseases. This article reviews different aspects mechanism including fusion fission, biogenesis, mitophagy, highlights therapy osteoporosis (diabetes induced postmenopausal osteoporosis) to novel targets prevention strategies for treatment other
Language: Английский
Citations
51Cell Metabolism, Journal Year: 2024, Volume and Issue: 36(2), P. 315 - 337
Published: Jan. 10, 2024
Language: Английский
Citations
20Developmental Cell, Journal Year: 2018, Volume and Issue: 44(2), P. 139 - 163
Published: Jan. 1, 2018
Language: Английский
Citations
144Aging Cell, Journal Year: 2017, Volume and Issue: 16(5), P. 934 - 942
Published: July 19, 2017
Cataract is one of the most important causes blindness worldwide, with age-related cataract being common one. Agents preventing formation are urgently required. Substantial evidences point out aggravated oxidative stress as a vital factor for formation. Nuclear (erythroid-derived 2)-like 2 (Nrf2)/Kelch-like erythroid-cell-derived protein CNC homology (ECH)-associated 1 (Keap1) system considered main cellular defense mechanisms against stresses. This review discusses role Nrf2 pathway in prevention cataracts and highlights that suppressors may augment lens, inducers decrease prevent Thus, serve promising therapeutic target treatment.
Language: Английский
Citations
109