Calcineurin (PPP3CB) regulates angiotensin II‐dependent vascular remodelling by potentiating EGFR signalling in mice

Abstract

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Transcriptome-wide analysis reveals the coregulation of RNA-binding proteins and alternative splicing genes in the development of atherosclerosis

“…Loss of Cβ2 can increase the inflammatory susceptibility of macrophages 57 , and Cβ2 transcripts were reduced in the advanced samples of this study, which may cause plaque progression. Angiotensin II-induced vascular smooth muscle exhibits increased PPP3CB-dependent extracellular matrix secretion, suggesting that PPP3CB destabilizes plaques during atherosclerosis 58 .…”

Exercise‐mediated autophagy in cardiovascular diseases

“…However, as atherosclerosis and pathological vascular remodeling progress as a hallmark of CVD progresses, autophagy is gradually impaired. [24][25][26][27] In the atherosclerosis model of mice with ApoE knockout and high-fat diet-fed, autophagy-related protein ATG5 and ATG12 were markedly decreased in CD31 positive endothelial cells from the aorta. Furthermore, the contraction of skeletal muscle during dynamic exercise requires an increase in blood flow to meet elevated oxygen demands.…”

“…In the early stages of atherosclerosis, autophagy has an important role in anti‐atherosclerosis by degrading and recycling cytotoxic components. However, as atherosclerosis and pathological vascular remodeling progress as a hallmark of CVD progresses, autophagy is gradually impaired 24–27 . In the atherosclerosis model of mice with ApoE knockout and high‐fat diet‐fed, autophagy‐related protein ATG5 and ATG12 were markedly decreased in CD31 positive endothelial cells from the aorta.…”

Prolyl hydroxylase inhibitors, polydrug use, and the phosphoproteome

“…The lack of activated T-cells leads to inhibition of the immune response and therefore prevents the rejection of transplanted organs. 16,17 While immunosuppression is crucial for graft survival, CsA exerts nephrotoxic effects, which should be taken into consideration. 5 The exact pathomechanism of CsA-induced nephrotoxicity is incompletely understood, but hypoxia may be involved.…”

“…IL‐2 is crucial for differentiation and modulation of T‐cells. The lack of activated T‐cells leads to inhibition of the immune response and therefore prevents the rejection of transplanted organs 16,17 …”