NDUFS3 alleviates oxidative stress and ferroptosis in sepsis induced acute kidney injury through AMPK pathway.

In recent years, ferroptosis has been found to play an important role in various acute kidney injury (AKI). However, relatively little research has been conducted on sepsis-induced acute kidney injury (SI-AKI). As an important trigger of ferroptosis, how mitochondrial damage plays a regulatory role in SI-AKI is still unclear.

Aquaporin-1 Facilitates Macrophage M1 Polarization by Enhancing Glycolysis Through the Activation of HIF1α in Lipopolysaccharide-Induced Acute Kidney Injury.

This study aimed to investigate how aquaporin 1 (AQP1) modulates hypoxia-inducible factor-1α (HIF1α) to promote glycolysis and drive the M1 polarization of macrophages. Within 12 h post-treatment with LPS to induce acute kidney injury in rats, a significant upregulation of AQP1 and HIF1α protein levels was noted in serum and kidney tissues. This elevation corresponded with a decrease in blood glucose concentrations and an enhancement of glycolytic activity relative to the control group.

BMP2 Diminishes Angiotensin II-Induced Atrial Fibrillation by Inhibiting NLRP3 Inflammasome Signaling in Atrial Fibroblasts.

Atrial fibrillation (AF) is the most common sustained arrhythmia to affect 1% of the global population and increases with age. Atrial fibrosis is a crucial substrate for promoting structural remodeling to cause atrial arrhythmogenesis. Bone morphogenic protein 2 (BMP2) has been reported to be involved in cardiac fibrogenesis.

IRF2BP2 prevents ox-LDL-induced inflammation and EMT in endothelial cells via regulation of KLF2.

Oxidized low-density lipoprotein (ox-LDL)-induced endothelial dysfunction contributes to the progression of atherosclerosis. Interferon regulatory factor 2-binding protein 2 (IRF2BP2) attenuates macrophage-mediated inflammation and susceptibility to atherosclerosis. However, the effects of IRF2BP2 on vascular endothelial cells in atherosclerosis have not been fully elucidated.

Upregulation of β3-adrenergic receptors contributes to atrial structural remodeling in rapid pacing induced atrial fibrillation canines.

Accumulating evidence suggests that the adrenergic receptors (ARs) play an important role in cardiac diseases. The expression of β3-AR has been recently demonstrated in atria, however, its role in atrial structural remodeling of atrial fibrillation (AF) is unclear. Therefore, the present study was designed to investigate the role of β3-AR in atrial structural remodeling in AF and to clarify its possible mechanisms.