ArticleScientific reports2022
Investigating the role of heat shock protein 47 in fibrosis in Crohn's disease.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Synergistic biocontrol of Parthenium hysterophorus: the role of Curvularia specifera and Zygogramma bicolorata.Archives of microbiology · 2026Article
- Comparative assessment of the effects of dotinurad and febuxostat on the renal function in chronic kidney disease patients with hyperuricemia.Scientific reports · 2025Article
- Article
- HSP47 in human diseases: Navigating pathophysiology, diagnosis and therapy.Clinical and translational medicine · 2024Review
- Inflammatory Bowel Diseases: An Updated Overview on the Heat Shock Protein Involvement.International journal of molecular sciences · 2023Review
- Identification of molecular mechanisms causing skin lesions of cutaneous leishmaniasis using weighted gene coexpression network analysis (WGCNA).Scientific reports · 2023Article
- Targeting HSP47 and HSP70: promising therapeutic approaches in liver fibrosis management.Journal of translational medicine · 2022Review
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Crohn's disease (CD) and ulcerative colitis (UC) are chronic inflammatory disorders of the gastrointestinal tract that share similar genetic risk factors. However, while fibrotic stricture of the intestine is a major characteristic of CD; it is rarely observed in UC. Deposition of collagen in the extracellular matrix contributes to the formation of fibrotic strictures in CD, but the underlying mechanisms are unknown. In the present study, we found that heat shock protein 47 (HSP47), a stress-response protein that acts as a molecular chaperone during the processing and secretion of collagen, expressed in the intestinal tissue from patients with CD. Serum HSP47 levels and anti-HSP47 antibody titers were significantly higher in patients with CD than in those with UC. Furthermore, anti-HSP47 antibody levels correlated significantly with fibrosis in CD. In addition, HSP47 inhibition significantly suppressed collagen production in fibroblasts in vitro. These findings suggest that HSP47 is a biomarker for differentiating fibrotic from non-fibrotic forms of CD. Additionally, we propose that HSP47 could be a potential target for treating fibrosis in patients with CD.
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