The fibrosis in IPF has been linked to cigarette smoking, environmental factors (e.g. occupational exposure to gases, smoke, chemicals or dust.), and other medical complications including gastro intestinal reflex disease (GERD) or to genetic predisposition (Familial IPF).
IPF is the result of an aberrant wound healing process including, involving abnormal & excessive deposition of ‘Collagen’ (Fibrosis) in the pulmonary interstitium with minimal associated ‘inflamation’.
When type I AECs are damaged or last, it is through basement membranes.
In normal repair, the hyperplastic type II AECs die & remaining cells spread & undergo a differentiation process to become type I AECs.
Under pathologic conditions & in the presence of transforming growth factor beta (TGFB), fibroblasts accumulate in these areas of damage & differentiate myofibroblasts that secret collagen & other proteins.
The development of fibroblastic foci precedes the accumulation of inflammatory cells & the consequent deposition of collagen.
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