Tag results:

AngII

Lipid Phosphate Phosphatase 3 in Smooth Muscle Cells Regulates Angiotensin II-Induced Abdominal Aortic Aneurysm Formation

[Scientific Reports] Investigators investigated the role of lipid phosphate phosphatase 3 and lysophospholipid signaling in a well-defined model of pathologic aortic injury.

Losartan Protects Human Stem Cell-Derived Cardiomyocytes from Angiotensin II-Induced Alcoholic Cardiotoxicity

[Cell Death Discovery] Investigators established an in vitro model of alcoholic cardiomyopathy based on human induced pluripotent stem cell-derived cardiomyocytes.

CCL17 Aggravates Myocardial Injury by Suppressing Recruitment of Regulatory T Cells

[Circulation] Investigators utilized mouse models of reperfused myocardial infarction, angiotensin II and phenylephrine infusion, and diphtheria toxin cardiomyocyte ablation to investigate C-C chemokine ligand 17.

Protective Effects of Endothelial Progenitor Cell Microvesicles on Ang II-Induced Rat Kidney Cell Injury

[Molecular Medicine Reports] Chronic hypertension can lead to kidney damage, known as hypertensive nephropathy or hypertensive nephrosclerosis. The authors investigated the mechanisms by which endothelial progenitor cells repaired primary rat kidney cells.

Long Noncoding RNA p21 Enhances Autophagy to Alleviate Endothelial Progenitor Cells Damage and Promote Endothelial Repair in Hypertension through SESN2/AMPK/TSC2 Pathway

[Pharmacological Research] The authors showed that the number of endothelial progenitor cells (EPCs) in hypertensive patients was significantly lower than that of normal population, and the cell function decreased with a higher proportion of EPCs at later stages.

Erythropoietin Promotes Abdominal Aortic Aneurysms in Mice through Angiogenesis and Inflammatory Infiltration

[Science Translational Medicine] Researchers found that erythropoietin (EPO) promoted the formation of abdominal aortic aneurysm (AAA) in both Apoe−/− and wild type mice by enhancing angiogenesis, inflammation, collagen degradation, and apoptosis of smooth muscle cells and that EPO/EPO receptor signaling was essential for angiotensin II-induced AAA.

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