Matches in SemOpenAlex for { <https://semopenalex.org/work/W2968897107> ?p ?o ?g. }
- W2968897107 endingPage "851" @default.
- W2968897107 startingPage "841" @default.
- W2968897107 abstract "Objective We evaluated the influence of the renin–angiotensin system (RAS) on intestinal inflammation and fibrosis. Design Cultured human colonic myofibroblast proliferation and collagen secretion were assessed following treatment with angiotensin (Ang) II and Ang (1–7), their receptor antagonists candesartan and A779, and the ACE inhibitor captopril. Circulating and intestinal RAS components were evaluated in patients with and without IBD. Disease outcomes in patients with IBD treated with ACE inhibitors and angiotensin receptor blockers (ARBs) were assessed in retrospective studies. Results Human colonic myofibroblast proliferation was reduced by Ang (1–7) in a dose-dependent manner (p<0.05). Ang II marginally but not significantly increased proliferation, an effect reversed by candesartan (p<0.001). Colonic myofibroblast collagen secretion was reduced by Ang (1–7) (p<0.05) and captopril (p<0.001), and was increased by Ang II (p<0.001). Patients with IBD had higher circulating renin (mean 25.4 vs 18.6 mIU/L, p=0.026) and ACE2:ACE ratio (mean 0.92 vs 0.69, p=0.015) than controls without IBD. RAS gene transcripts and peptides were identified in healthy and diseased bowels. Colonic mucosal Masson’s trichrome staining correlated with Ang II (r=0.346, p=0.010) and inversely with ACE2 activity (r=−0.373, p=0.006). Patients with IBD who required surgery (1/37 vs 12/75, p=0.034) and hospitalisation (0/34 vs 8/68, p=0.049) over 2 years were less often treated with ACE inhibitors and ARBs than patients not requiring surgery or hospitalisation. Conclusions The RAS mediates fibrosis in human cell cultures, is expressed in the intestine and perturbed in intestinal inflammation, and agents targeting this system are associated with improved disease outcomes." @default.
- W2968897107 created "2019-08-22" @default.
- W2968897107 creator A5008098216 @default.
- W2968897107 creator A5014298155 @default.
- W2968897107 creator A5021391324 @default.
- W2968897107 creator A5024943696 @default.
- W2968897107 creator A5029917190 @default.
- W2968897107 creator A5030190044 @default.
- W2968897107 creator A5032091930 @default.
- W2968897107 creator A5034194893 @default.
- W2968897107 creator A5035437527 @default.
- W2968897107 creator A5035759710 @default.
- W2968897107 creator A5039484371 @default.
- W2968897107 creator A5042898422 @default.
- W2968897107 creator A5049864741 @default.
- W2968897107 creator A5053331129 @default.
- W2968897107 creator A5061386726 @default.
- W2968897107 creator A5071293171 @default.
- W2968897107 creator A5077991733 @default.
- W2968897107 creator A5078868987 @default.
- W2968897107 creator A5080941710 @default.
- W2968897107 creator A5081705050 @default.
- W2968897107 creator A5084329889 @default.
- W2968897107 creator A5088957393 @default.
- W2968897107 creator A5090214501 @default.
- W2968897107 date "2019-08-13" @default.
- W2968897107 modified "2023-09-27" @default.
- W2968897107 title "Imbalance of the renin–angiotensin system may contribute to inflammation and fibrosis in IBD: a novel therapeutic target?" @default.
- W2968897107 cites W1516304808 @default.
- W2968897107 cites W1549188344 @default.
- W2968897107 cites W1950141864 @default.
- W2968897107 cites W1966339428 @default.
- W2968897107 cites W1968719631 @default.
- W2968897107 cites W1974901207 @default.
- W2968897107 cites W1990544851 @default.
- W2968897107 cites W1997581872 @default.
- W2968897107 cites W1997702183 @default.
- W2968897107 cites W2005398267 @default.
- W2968897107 cites W2017614891 @default.
- W2968897107 cites W2024734303 @default.
- W2968897107 cites W2026508510 @default.
- W2968897107 cites W2035804355 @default.
- W2968897107 cites W2038578669 @default.
- W2968897107 cites W2038737915 @default.
- W2968897107 cites W2045397597 @default.
- W2968897107 cites W2056771634 @default.
- W2968897107 cites W2068475055 @default.
- W2968897107 cites W2071658329 @default.
- W2968897107 cites W2073647905 @default.
- W2968897107 cites W2080775326 @default.
- W2968897107 cites W2115360097 @default.
- W2968897107 cites W2116318925 @default.
- W2968897107 cites W2130567407 @default.
- W2968897107 cites W2135403010 @default.
- W2968897107 cites W2137576770 @default.
- W2968897107 cites W2161399617 @default.
- W2968897107 cites W2163633813 @default.
- W2968897107 cites W2167384912 @default.
- W2968897107 cites W2169068394 @default.
- W2968897107 cites W2169843939 @default.
- W2968897107 cites W2181701210 @default.
- W2968897107 cites W2295658637 @default.
- W2968897107 cites W2313203176 @default.
- W2968897107 cites W2585608783 @default.
- W2968897107 cites W2592131189 @default.
- W2968897107 cites W2593695507 @default.
- W2968897107 cites W2745643218 @default.
- W2968897107 cites W2809196018 @default.
- W2968897107 cites W2896255162 @default.
- W2968897107 cites W3217532623 @default.
- W2968897107 cites W4243637399 @default.
- W2968897107 doi "https://doi.org/10.1136/gutjnl-2019-318512" @default.
- W2968897107 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31409604" @default.
- W2968897107 hasPublicationYear "2019" @default.
- W2968897107 type Work @default.
- W2968897107 sameAs 2968897107 @default.
- W2968897107 citedByCount "145" @default.
- W2968897107 countsByYear W29688971072020 @default.
- W2968897107 countsByYear W29688971072021 @default.
- W2968897107 countsByYear W29688971072022 @default.
- W2968897107 countsByYear W29688971072023 @default.
- W2968897107 crossrefType "journal-article" @default.
- W2968897107 hasAuthorship W2968897107A5008098216 @default.
- W2968897107 hasAuthorship W2968897107A5014298155 @default.
- W2968897107 hasAuthorship W2968897107A5021391324 @default.
- W2968897107 hasAuthorship W2968897107A5024943696 @default.
- W2968897107 hasAuthorship W2968897107A5029917190 @default.
- W2968897107 hasAuthorship W2968897107A5030190044 @default.
- W2968897107 hasAuthorship W2968897107A5032091930 @default.
- W2968897107 hasAuthorship W2968897107A5034194893 @default.
- W2968897107 hasAuthorship W2968897107A5035437527 @default.
- W2968897107 hasAuthorship W2968897107A5035759710 @default.
- W2968897107 hasAuthorship W2968897107A5039484371 @default.
- W2968897107 hasAuthorship W2968897107A5042898422 @default.
- W2968897107 hasAuthorship W2968897107A5049864741 @default.
- W2968897107 hasAuthorship W2968897107A5053331129 @default.
- W2968897107 hasAuthorship W2968897107A5061386726 @default.
- W2968897107 hasAuthorship W2968897107A5071293171 @default.