Erratum to: Angiotensin II stimulates canonical TGF-β signaling pathway through angiotensin type 1 receptor to induce granulation tissue contraction

Abstract

. Furthermore, Licheng Ren shares first authorship with Tosan Ehanire.The online version of the original article can be found at http://dx

Molecular Insights Into SARS COV-2 Interaction With Cardiovascular Disease: Role of RAAS and MAPK Signaling

“…Furthermore, this protease is regulated by ERK pathways under inflammatory conditions (Ventura et al, 2017). In fact, ERK1 is essential for maintaining activity of furin and has been implicated as a -↑AngII!↑mechanisms involving growth factor receptors (e.g., PDGF and TGF-b receptors) !↑ERK activation cardiac and vascular hypertrophy and fibrosis (Schellings et al, 2006;Ehanire et al, 2015) -↑AngII activity in CVD!↓cell surface expression of ACE2 in an AT 1 /p38 MAPK-dependent pathway leading to protein excision and shedding (Patel et al, 2014;Xu et al, 2017) ↑AngII/AT 1 R pathway!↑MAPK signaling!↑signs of CVD -ACE2 deletion!↑NADPH oxidase activity, superoxide generation, MAPK signaling and inflammatory cytokine production in the aorta of mice receiving AngII (Jin et al, 2012) -↑ACE2/Ang-(1-7)pathway!↓AngII-induced inflammation in cardiac tissue and in hypothalamic cardiovascular centers, cardiac remodeling, and hypertension (Grobe et al, 2007;Sriramula et al, 2011) ↑ACE2/Ang(1-7) pathway!↓MAPK signaling!↓ inflammation!amelioration of CVD -ACE2 overexpression !↓TNF-a, IL-1b, and IL-6 in and ↑antiinflammatory cytokine IL-10 in autoimmune myocarditis (Sukumaran et al, 2011) Contribution of MAPK signaling to CVD -Erk1/2. JNK, and p38 MAPK activation !↑cardiomyopathic remodeling (Wang, 2007) -Pressure overload!↑Ras/c-RAF/MKK1/ERK1/2 pathway!cardiac hypertrophy, ↑cardiomyocyte size, diastolic dysfunction, and myofibril disarray (Hunter et al, 1995) -ERK1/2 !↑ c-Fos !↑ GLUT1 transporter expression in hypertrophic and ischemic heart (Babu et al, 2000) (Santalucia et al, 2003) (Shao and Tian, 2015) -MAPK pathway activation!progressive endothelial dysfunction (Huang et al, 2012) -Oxidized LDL!↑ MAPK pathway activation!↑GM-CSF!↑macrophage infiltration of atherosclerotic plaques (Proctor et al, 2007;Muslin, 2008) -↑MAPK pathway activation!↑interleukins and TNFa!↑atherosclerotic lesion progression (Bachstetter and Van Eldik, 2010;De Souza et al, 2014) -TNFa!↑ERK1/2 activity!↑MMP9 !↑fibrotic lesion formation (Cheng et al, 2012;Zhang et al, 2017) -Viral infection!↑IL-1, TNFa, IL-6!↑p38 MAPK and JNK !↑viral cardiomyopathy (Monsuez et al, 2007;Wang et al, 2014;…”

Contribution of TGF-Beta-Mediated NLRP3-HMGB1 Activation to Tubulointerstitial Fibrosis in Rat With Angiotensin II-Induced Chronic Kidney Disease

“…It is the main effector of the renin angiotensin aldosterone system (RAAS), and increasing its levels can promote RAAS activity, resulting in severe vascular, glomerular, and tubulointerstitial injuries along with the release of the cytokine TGF-beta through the angiotensin type 1 receptor (Balakumar et al, 2019). TGFbeta is required for Ang II to activate fibroblasts and induce fibrosis (Ehanire et al, 2015b;Angelov et al, 2017). In CKD, targeting fibrotic progression may reduce kidney injury and improve the efficiency of treatment strategies based on cellular studies.…”