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fibrosis
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:
- idiopathic pulmonary fibrosis
- scleroderma
- cirrhosis
- myelofibrosis [1]
- 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]
Specific
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
General
pathologic process
sign/symptom
References
- 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: 28424250
- 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: 28416697