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Drp1-Dependent Mitochondrial Fission Contributes to Lactic Acid-Induced Chicken Cardiomyocyte Damage.
J Biochem Mol Toxicol
January 2025
College of Animal Science and Technology, Henan Institute of Science and Technology, Xinxiang, China.
Enhanced glycolysis and elevated lactic acid (LA) production are observed during sudden death syndrome (SDS) in broilers. However, the mechanism underlying LA-induced cardiomyocyte damage and heart failure in fast-growing broilers remains unclear. In this study, chicken embryo cardiomyocytes (CECs) were cultured and treated with LA to investigate LA-induced CEC injury and its mechanism, aiming to develop strategies to prevent LA-induced SDS in broilers.
View Article and Find Full Text PDFNuclear receptor 4A1 Regulates Mitochondrial Homeostasis in Cardiac Post-Ischemic Injury by Controlling Mitochondrial Fission 1 Protein-Mediated Fragmentation and Parkin-Dependent Mitophagy.
Int J Biol Sci
January 2025
Department of Cardiovascular Surgery, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China 510120.
Article Synopsis
- Mitochondrial fission and mitophagy are crucial for understanding myocardial ischemia-reperfusion (IR) injury, but their regulatory mechanisms are not well understood.
- Elevated Nr4a1 levels after myocardial IR injury correlate with worse cardiac function, increased cell death, inflammation, and endothelial issues, while Nr4a1-knockout mice show protection and better mitochondrial health.
- Targeting Nr4a1 to balance mitochondrial fission and mitophagy could provide new therapeutic options to improve heart health during ischemic conditions.
Exploiting Mitochondria by Triggering a Faulty Unfolded Protein Response Leads to Effective Cardioprotection.
Int J Med Sci
January 2025
Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China.
This study investigates the role of Fundc1 in cardiac protection under high-altitude hypoxic conditions and elucidates its underlying molecular mechanisms. Using cardiomyocyte-specific knockout ( ) mice, we demonstrated that deficiency exacerbates cardiac dysfunction under simulated high-altitude hypoxia, manifesting as impaired systolic and diastolic function. Mechanistically, we identified that Fundc1 regulates cardiac function through the mitochondrial unfolded protein response (mito-UPR) pathway.
View Article and Find Full Text PDFMitophagy in ischemic heart disease: molecular mechanisms and clinical management.
Cell Death Dis
December 2024
Xiyuan Hospital of China Academy of Chinese Medical Sciences, Beijing, 100091, China.
The influence of the mitochondrial control system on ischemic heart disease has become a major focus of current research. Mitophagy, as a very crucial part of the mitochondrial control system, plays a special role in ischemic heart disease, unlike mitochondrial dynamics. The published reviews have not explored in detail the unique function of mitophagy in ischemic heart disease, therefore, the aim of this paper is to summarize how mitophagy regulates the progression of ischemic heart disease.
View Article and Find Full Text PDFMETTL3, m6A modification, and EGR1: interplay affecting myocardial I/R injury outcomes.
Cell Biol Toxicol
December 2024
Department of Cardiovascular Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450000, China.
The occurrence of severe myocardial ischemia/reperfusion (I/R) injury is associated with the clinical application of reestablishment technique for heart disease, and understanding its underlying mechanisms is currently an urgent issue. Prior investigations have demonstrated the potential enhancement of MIRI through EGR1 suppression, although the precise underlying regulatory pathways require further elucidation. The core focus of this investigation is to examine the molecular pathways through EGR1 regulates mitophagy-mediated myocardial cell pyroptosis and its impact on MIRI.
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