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

Baicalin attenuates the immune escape of oral squamous cell carcinoma by reducing lactate accumulation in tumor microenvironment DOI Creative Commons

Yameng Cui,

Jingwen Liu, Xi Wang

et al.

Journal of Advanced Research, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 1, 2025

Language: Английский

Citations

3
M6a demethylase FTO regulates the oxidative stress, mitochondrial biogenesis of cardiomyocytes and PGC-1a stability in myocardial ischemia-reperfusion injury DOI Creative Commons
Qiong Jiang, Xuehai Chen,

Kezeng Gong

et al.

Redox Report, Journal Year: 2025, Volume and Issue: 30(1)

Published: Jan. 27, 2025

Myocardial ischemia-reperfusion injury (MIRI) is a highly complex disease with high morbidity and mortality. Studying the molecular mechanism of MIRI discovering new targets are crucial for future treatment MIRI. We constructed rat model hypoxia/reoxygenation (H/R) cardiomyocytes model. RT-PCR Western blot were used to investigate expression fat mass obesity-associated (FTO) gene. Electrocardiogram, echocardiography, triphenyltetrazolium chloride (TTC) staining hematoxylin-eosin (HE) assess effect FTO overexpression. The generation reactive oxygen species (ROS) levels superoxide dismutase (SOD2), mitochondrial transcription factor (TFAM) cytochrome c oxidase I (COXI) detected oxidative stress biogenesis. RNA immunoprecipitation (RIP) pulldown assays identify interaction PGC-1a. m6A dot blot, methylated PCR (MeRIP-PCR) stability analysis analyze regulation methylation PGC-1a by FTO. was downregulated in rats H/R induced cardiomyocytes. Overexpression inhibited ROS level increased SOD2, TFAM COXI vitro vivo. In addition, identified as downstream target enhanced mRNA through removing modification. Our study revealed role regulates biogenesis via MIRI, which may provide approach mitigating

Language: Английский

Citations

1
Transcriptome reveals Gafmt-1 and Gadlc-1–5 play positive roles in cotton resistance to Verticillium wilt DOI
Jiale Chen, Susu Liu,

Guoli Feng

et al.

Plant Cell Reports, Journal Year: 2025, Volume and Issue: 44(4)

Published: March 18, 2025

Language: Английский

Citations

0
Roles of Autophagy, Mitophagy, and Mitochondria in Left Ventricular Remodeling after Myocardial Infarction DOI Creative Commons

Xin Zhang,

Shuai Shao,

Qiuting Li

et al.

Reviews in Cardiovascular Medicine, Journal Year: 2025, Volume and Issue: 26(3)

Published: March 24, 2025

This review examines the mechanisms of left ventricular dysfunction, focusing on interplay between remodeling, autophagy, and mitochondrial dysfunction following myocardial infarction. Left directly affects heart's pumping efficiency can lead to severe clinical outcomes, including heart failure. After infarction, ventricle may suffer from weakened contractility, diastolic cardiac progressing Thus, this article discusses pathophysiological processes involved in injury repair infarcted non-infarcted myocardia, adaptive changes, specific changes systolic functions. Furthermore, role autophagy maintaining cellular energy homeostasis, clearing dysfunctional mitochondria, key failure is addressed. Finally, therapeutic strategies targeting enhancing mitophagy, providing clinicians researchers with latest insights future research directions.

Language: Английский

Citations

0
METTL5 triggers the ferroptosis of cardiomyocytes in sepsis-induced myocardial injury DOI
Xiaoye Wang, Qi Tian, Miaomiao Li

et al.

Free Radical Biology and Medicine, Journal Year: 2025, Volume and Issue: unknown

Published: May 1, 2025

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