p22phox promotes Ang-II-induced vascular smooth muscle cell phenotypic switch by regulating KLF4 expression

NADPH oxidase in the vasculature: Expression, regulation and signalling pathways; role in normal cardiovascular physiology and its dysregulation in hypertension

“…Several studies have examined the effects of knockout, siRNA depletion or over-expression of NOX isoforms or regulatory subunits on blood pressure, associated functional abnormalities and signalling in various mouse or rat models of hypertension. Ang II-induced hypertension and associated increases in ROS production, ERK phosphorylation, proliferation and migration are blunted in p47 phox-/mice [41,72,72,104,166] or by p22 phox siRNA or antisense [61,157,560], while the hypertrophic response is enhanced by over-expressing p22 phox [552]. p22 phox-/or p22 phox siRNA also reduce MAP in salt-loaded strokeprone SHR [561] or Ang II-induced hypertension [61,157].…”

Tissue engineered in-vitro vascular patch fabrication using hybrid 3D printing and electrospinning

“…Here we used TGFβ1, PDGF-BB, and BMP4 for inducing the differentiation of MSC into dVSMC. Other authors bet using vasoactive peptides [ [77] , [78] , [79] ], pleitropic lysophospholipids [ 80 ], heparin [ 81 ] and so on.…”

Exosomal LINC01005 derived from oxidized low‐density lipoprotein‐treated endothelial cells regulates vascular smooth muscle cell phenotypic switch

“…KLF4, a zinc finger‐containing transcription factor, has been shown as an important regulator of the VSMC phenotypic switch and proliferation 19,20 . Shankman et al postulated that conditional knockout of KLF4 within SMCs resulted in phenotypic transitions that are favorable for atherosclerotic plaque pathogenesis in a mouse model of AS 25 .…”