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| http://dx.doi.org/10.1161/CIRCULATIONAHA.123.065507 | DOI Listing |
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Circ_0001084/miR-181c-5p/PTPN4 Axis Mitigates Cardiomyocyte Injury by Modulating the TLR4/NF-κB Pathway: Insights into Therapeutic Potential for Myocardial Reperfusion Injury.
J Inflamm Res
January 2025
Department of Hepatobiliary Surgery, The First People's Hospital of Zhaoqing, Zhaoqing City, Guangdong Province, People's Republic of China.
Background: Myocardial ischemia/reperfusion (I/R) injury significantly impacts the recovery of ischemic heart disease patients. Non-coding RNAs, including miRNAs, have been increasingly recognized for their roles in regulating cardiomyocyte responses to hypoxia/reoxygenation (H/R) injury. miR-181c-5p, in particular, has been implicated in inflammatory and apoptotic processes, suggesting its potential involvement in exacerbating cellular damage.
View Article and Find Full Text PDFDownregulation of HDAC2 attenuates ventricular arrhythmias in a mouse model of cardiac hypertrophy through upregulation of KCHIP2 expression.
Cardiovasc Res
January 2025
Department of Pathophysiology, Shenzhen University Medical School, Shenzhen 518060, China.
Aims: Decrease in repolarizing K+ currents, particularly the fast component of transient outward K+ current (Ito,f), prolongs action potential duration (APD) and predisposes the heart to ventricular arrhythmia during cardiac hypertrophy. Histone deacetylases (HDACs) have been suggested to participate in the development of cardiac hypertrophy, and class I HDAC inhibition has been found to attenuate pathological remodeling. This study investigated the potential therapeutic effects of HDAC2 on ventricular arrhythmia in pressure overload-induced cardiac hypertrophy.
View Article and Find Full Text PDFM6a demethylase FTO regulates the oxidative stress, mitochondrial biogenesis of cardiomyocytes and PGC-1a stability in myocardial ischemia-reperfusion injury.
Redox Rep
December 2025
Department of Cardiology, Fujian Medical University Union Hospital, Fuzhou, Fujian, People's Republic of China.
Objective: Myocardial ischemia-reperfusion injury (MIRI) is a highly complex disease with high morbidity and mortality. Studying the molecular mechanism of MIRI and discovering new targets are crucial for the future treatment of MIRI.
Methods: We constructed the MIRI rat model and hypoxia/reoxygenation (H/R) injury cardiomyocytes model.
Assembly of ceria-Nrf2 nanoparticles as macrophage-targeting ROS scavengers protects against myocardial infarction.
Front Pharmacol
January 2025
The Sixth Affiliated Hospital, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Molecular Target and Clinical Pharmacology, the NMPA and State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences, Guangzhou Medical University, The Fifth Affiliated Hospital, Guangzhou, China.
Myocardial infarction (MI) is a leading cause of morbidity and mortality worldwide, and mitigating oxidative stress is crucial in managing MI. Nuclear factor erythroid 2-related factor 2 (Nrf2) plays a critical role in combating oxidative stress and facilitating cardiac remodeling post-MI. Here, we engineered Cerium oxide (CeO) nanoparticle-guided assemblies of ceria/Nrf2 nanocomposites to deliver Nrf2 plasmids.
View Article and Find Full Text PDFDynamic map illuminates Hippo-cMyc module crosstalk driving cardiomyocyte proliferation.
Development
January 2025
Department of Biomedical Engineering, University of Virginia, Charlottesville, VA, Albemarle.
Numerous regulators of cardiomyocyte (CM) proliferation have been identified, yet how they coordinate during cardiac development or regeneration is poorly understood. Here, we developed a computational model of the CM proliferation regulatory network to obtain key regulators and systems-level understanding. The model defines five modules (DNA replication, mitosis, cytokinesis, growth factor, Hippo pathway) and integrates them into a network of 72 nodes and 88 reactions that correctly predicts 73 of 78 (93.
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