Mitophagy in Doxorubicin-Induced Cardiotoxicity: Insights into Molecular Biology and Novel Therapeutic Strategies DOI Creative Commons
Heng Zhang, Saiyang Xie, Wei Deng

et al.

Biomolecules, Journal Year: 2024, Volume and Issue: 14(12), P. 1614 - 1614

Published: Dec. 17, 2024

Doxorubicin is a chemotherapeutic drug utilized for solid tumors and hematologic malignancies, but its clinical application hampered by life-threatening cardiotoxicity, including cardiac dilation heart failure. Mitophagy, cargo-specific form of autophagy, specifically used to eliminate damaged mitochondria in autophagosomes through hydrolytic degradation following fusion with lysosomes. Recent advances have unveiled major role defective mitophagy the etiology DOX-induced cardiotoxicity. Moreover, specific interventions targeting this mechanism preserve mitochondrial function emerged as potential therapeutic strategies attenuate However, translation challenging because unclear mechanisms action pharmacological adverse effects. This review aims offer fresh perspectives on development cardiotoxicity investigate that focus improve management.

Language: Английский

Senolytic treatment alleviates cochlear senescence and delays age-related hearing loss in C57BL/6J mice DOI
Yi Chen, Hongming Huang,

Yuelian Luo

et al.

Phytomedicine, Journal Year: 2025, Volume and Issue: unknown, P. 156772 - 156772

Published: April 1, 2025

Language: Английский

Citations

0

The associations between brain aging and mitochondria dysfunction: Mechanism and intervention strategies DOI
Yi Rong

Deleted Journal, Journal Year: 2025, Volume and Issue: unknown, P. 1 - 16

Published: April 20, 2025

Brain aging, an exquisitely intricate biological phenomenon, is intertwined with cognitive deterioration and the pathogenesis of neurodegenerative maladies. Mitochondria, cellular powerhouses responsible for energy homeostasis, assume a central indispensable role in this process. This review delves deeply into multifaceted associations between mitochondrial dysfunction brain encompassing perturbations metabolism, exacerbation oxidative stress, aberrations dynamics, activation inflammatory response, DNA mutations, all which interact complex network to drive progression aging. Simultaneously, it undertakes meticulous dissection functions some key mitochondria-related molecules In terms intervention strategies, emerging evidence suggests that inhibition cyclic GMP-AMP synthase-stimulator interferon genes (cGAS-STING) signaling axis holds promise alleviating phenotypes senescent cells tissues. Downregulating levels relevant transfer RNA-derived small RNAs (tsRNAs) represents potential approach safeguard crucial processes. Supplementation spermidine spermine has demonstrated efficacy ameliorating function performance. Moreover, comprehensive paradigms targeting antioxidative stress responses, autophagy regulation offer avenues retarding Collectively, existing body research furnishes profound insights underlying mechanisms aging serves as bedrock development efficacious modalities. Future imperatives should center on elucidating molecular mechanisms, formulating highly precise expediting translation basic findings clinical applications. utmost significance enhancing quality life elderly forestalling onset diseases.

Language: Английский

Citations

0

Mitophagy in Doxorubicin-Induced Cardiotoxicity: Insights into Molecular Biology and Novel Therapeutic Strategies DOI Creative Commons
Heng Zhang, Saiyang Xie, Wei Deng

et al.

Biomolecules, Journal Year: 2024, Volume and Issue: 14(12), P. 1614 - 1614

Published: Dec. 17, 2024

Doxorubicin is a chemotherapeutic drug utilized for solid tumors and hematologic malignancies, but its clinical application hampered by life-threatening cardiotoxicity, including cardiac dilation heart failure. Mitophagy, cargo-specific form of autophagy, specifically used to eliminate damaged mitochondria in autophagosomes through hydrolytic degradation following fusion with lysosomes. Recent advances have unveiled major role defective mitophagy the etiology DOX-induced cardiotoxicity. Moreover, specific interventions targeting this mechanism preserve mitochondrial function emerged as potential therapeutic strategies attenuate However, translation challenging because unclear mechanisms action pharmacological adverse effects. This review aims offer fresh perspectives on development cardiotoxicity investigate that focus improve management.

Language: Английский

Citations

1