Exendin-4 Prevents oxLDL-Induced upregulation of TREM2 and attenuates foam cell formation and inflammation in Macrophages.

Atherosclerosis (AS), a chronic inflammatory disease and a leading cause of cardiovascular morbidity and mortality. Macrophage-mediated lipid uptake and inflammation are central to plaque formation. TREM2, an immunoreceptor expressed in macrophages, has been reported to regulate lipid metabolism and inflammation, yet its role in atherosclerosis remains controversial.

2-aminoethoxydiphenylborane intervenes intracellular calcium signaling and attenuates myocardial ischemia-reperfusion injury in mice through ITPR1/MCU pathway.

Myocardial ischemia-reperfusion (MI/R) injury frequently occurs during the clinical management of ischemic heart disease. The underlying mechanism includes neutrophil infiltration, heightened intracellular Ca levels, mitochondrial energy metabolism disorder. This study investigated the pathological role of the inositol 1,4,5-trisphosphate receptor/mitochondrial calcium uniporter (ITPR1/MCU) pathway in regulating disturbances in intracellular calcium ([Ca]) and mitochondrial calcium ([Ca]) levels during MI/R injury.

Identification and experimental validation of KMO as a critical immune-associated mitochondrial gene in unstable atherosclerotic plaque.

Background: The heightened risk of cardiovascular and cerebrovascular events is associated with the increased instability of atherosclerotic plaques. However, the lack of effective diagnostic biomarkers has impeded the assessment of plaque instability currently. This study was aimed to investigate and identify hub genes associated with unstable plaques through the integration of various bioinformatics tools, providing novel insights into the detection and treatment of this condition.

PCSK9 regulates myofibroblast transformation through the JAK2/STAT3 pathway to regulate fibrosis after myocardial infarction.

Cardiac fibrosis is pivotal in the progression of numerous cardiovascular diseases. This phenomenon is hallmarked by an excessive deposition of ECM protein secreted by myofibroblasts, leading to increased myocardial stiffness. Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a serine protease that belongs to the proprotein-converting enzyme family.

Effect on hypoxia/reoxygenation-induced cardiomyocyte injury and Pink1/Parkin pathway.

Our study aimed to detect the effects of proprotein convertase subtilisin/kexin type 9 (PCSK9) on exacerbating cardiomyocyte hypoxia/reoxygenation (H/R) injury and the possible mechanism. A cell model of H/R was constructed. PCSK9 mRNA and protein levels were significantly upregulated during AC16 cardiomyocyte H/R.

PCSK9 Knockdown Can Improve Myocardial Ischemia/Reperfusion Injury by Inhibiting Autophagy.

This study investigates the effect and mechanism of proprotein convertase subtilisin/Kexin type 9 (PCSK9) on myocardial ischemia-reperfusion injury (MIRI) and provides a reference for clinical prevention and treatment of acute myocardial infarction (AMI). We established a rat model of myocardial ischemia/reperfusion (I/R) and AC16 hypoxia/reoxygenation (H/R) model. A total of 48 adult 7-week-old male Sprague-Dawley rats were randomly assigned to three groups (n = 16): control, I/R, and I/R + SiRNA.

Influence of static electric field on cognition in mice.

With the rapid development of high voltage direct current transmission, the possibility of health effects associated with static electric field (SEF) has caused wide public concern. To examine the effects of long-lasting, full-body exposure to SEF on cognition, Institute of Cancer Research mice were exposed to SEF for 35 d. The intensities of SEF in experimental group I (EG-I), experimental group II (EG-II) and control group (CG) were 2.