fibrosis
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Introduction
reactive process with proliferation of fibroblasts.
Pathology
- c-jun protein is produced in high amounts in end-stage fibrosis of many organs in both mice & humans, including:
- c-jun protein converts cells into pathologic fibroblasts, stimulates fibroblast proliferation, & causes the wayward fibroblasts to produce a molecule that protects them from destruction by macrophages[1]
Management
- itraconazole inhibits formtion of fibroblasts causing fibrosis[2]
More general terms
More specific terms
- angiofibrosis
- dihydropyrimidine dehydrogenase deficiency; hereditary thymine-uraciluria; familial pyrimidinemia
- fibroelastosis
- fibrosing colonopathy
- hepatic fibrosis
- mediastinal fibrosis (fibrosing mediastinitis)
- myelofibrosis
- myocardial fibrosis
- myofibrosis
- plantar fascial fibromatosis; Ledderhose's disease
- pulmonary fibrosis
- renal fibrosis
- retroperitoneal fibrosis (Ormond disease)
- storiform fibrosis
References
- ↑ 1.0 1.1 1.2 Wernig G, Chen SY, Cui L et al. Unifying mechanism for different fibrotic diseases. Proc Natl Acad Sci U S A 2017 May 2; 114:4757. PMID: https://www.ncbi.nlm.nih.gov/pubmed/28424250
- ↑ 2.0 2.1 Bollong MJ, Yang B, Vergani N et al. Small molecule-mediated inhibition of myofibroblast transdifferentiation for the treatment of fibrosis. Proc Natl Acad Sci U S A 2017 May 2; 114:4679. PMID: https://www.ncbi.nlm.nih.gov/pubmed/28416697