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| http://dx.doi.org/10.4070/kcj.2024.0114 | DOI Listing |
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Recombinant dsAAV9-mediated Endogenous Overexpression of Macrophage Migration Inhibitory Factor Alleviates Myocardial Ischemia-Reperfusion Injury via Activating AMPK and ERK1/2 Signaling Pathways.
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State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, First Affiliated Hospital of Xinjiang Medical University, Clinical Medical Research Institute, Xinjiang Medical University, No. 137 Liyushan South Road, Urumqi, 830054, China.
Purpose: To investigate the protective effect and mechanism of enhanced expression of endogenous macrophage migration inhibitory factor (MIF) on cardiac ischemia-reperfusion (I/R) injury.
Methods: A recombinant double-stranded adeno-associated virus serotype 9 with MIF or green fluorescent protein (GFP) genes (dsAAV9-MIF/GFP) was transduced into mice and neonatal rat ventricular myocytes (NRVMs). The models of cardiac 60 min ischemia and 24 h reperfusion and 12 h hypoxia/12 h reoxygenation (H/R) were established in mice and NRVMs, respectively.
Nuclear receptor 4A1 Regulates Mitochondrial Homeostasis in Cardiac Post-Ischemic Injury by Controlling Mitochondrial Fission 1 Protein-Mediated Fragmentation and Parkin-Dependent Mitophagy.
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Department of Cardiovascular Surgery, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China 510120.
The close interaction of mitochondrial fission and mitophagy, two crucial mechanisms, is key in the progression of myocardial ischemia-reperfusion (IR) injury. However, the upstream regulatory mechanisms governing these processes remain poorly understood. Here, we demonstrate a marked elevation in Nr4a1 expression following myocardial IR injury, which is associated with impaired cardiac function, heightened cardiomyocyte apoptosis, exacerbated inflammatory responses, and endothelial dysfunction.
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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.
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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 PDFExploring the molecular mechanisms of comorbidity of myocardial infarction and anxiety disorders by combining multiple data sets with in vivo experimental validation.
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December 2024
Dongfang Hospital of Beijing University of Chinese Medicine, Beijing, China. Electronic address:
Background: The incidence of comorbidity between myocardial infarction (MI) and anxiety disorders is increasing. However, the biological association between them has not been fully understood.
Objective: This study aims to investigate the molecular mechanisms of comorbidity between MI and anxiety disorders and to predict their key genes and potential therapeutic drugs.
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