Open AccessNr4A1 modulates inflammation-associated intestinal fibrosis and dampens fibrogenic signaling in myofibroblasts
Author(s) -
Vivek Krishna Pulakazhi Venu,
Laurie Alston,
Mircea Iftinca,
Yi-Cheng Tsai,
Matthew Stephens,
Vineetha Warriyar,
Sonia Rehal,
Grace Hudson,
H Szczepanski,
PierreYves von der Weid,
Christophe Altier,
Simon A. Hirota
Publication year - 2021
Publication title -
american journal of physiology. gastrointestinal and liver physiology/american journal of physiology: gastrointestinal and liver physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.644
H-Index - 169
eISSN - 1522-1547
pISSN - 0193-1857
DOI - 10.1152/ajpgi.00338.2019
Subject(s) - fibrosis , myofibroblast , medicine , inflammation , thickening , inflammatory bowel disease , complication , downregulation and upregulation , disease , gastroenterology , pathology , biology , chemistry , biochemistry , gene , polymer science
Fibrosis and increased muscle thickening contribute to stricture formation and intestinal obstruction, a complication that occurs in 30%–50% of patients with CD within 10 yr of disease onset. More than 50% of those who undergo surgery to remove the obstructed bowel will experience stricture recurrence. To date, there are no drug-based approaches approved to treat intestinal strictures. In the current submission, we identify NR4A1 as a novel target to treat inflammation-associated intestinal fibrosis.