Signaling mechanisms by which mitochondria regulates fibrosis in the lung
Description: PUBLIC HEALTH RELEVANCE: Idiopathic Pulmonary Fibrosis (IPF) is a fatal and progressive lung disease of unknown etiology, whose prevalence dramatically increases with age. The mechanisms that underlie the effects of advanced age remain unexplained. Similar to age-related neurodegenerative disease that has an etiology related to mitochondria dysfunction, we found that lung epithelial cells from aging and IPF lungs contain dysfunctional mitochondria that increases the vulnerability to cell death and fibrosis. Our research will unravel key mechanisms that control the expression of PINK1, a critical regulator of mitochondria homeostasis that is diminished in the IPF lung, and how mitochondria dysfunction lead to leakage of mtDNA that induces pro-fibrotic responses. These studies will allow us to identify therapeutic targets and to develop novel therapeutic strategies for IPF
Funding type: research
Funder scheme: R01
Start date: 2016-04-01
End date: 2021-03-31
Investigator: ANA LUCIA MORA
Institution: UNIVERSITY OF PITTSBURGH AT PITTSBURGH
Subfield: Pulmonary and Respiratory Medicine
Field: Medicine
Domain: Health Sciences
Funded outputs count: 25
Funder award ID: R01HL131789
OpenAlex ID: G1739728354