RIP3 activation by aging accelerates cigarette smoking-induced COPD
Description: Chronic Obstructive Pulmonary Disease (COPD) is a major cause of death and disability in the United States, particularly among older adults. While cigarette smoking is a well-known risk factor, how aging worsens smoking-related lung damage remains unclear. Recent research highlights necroptosis—a form of inflammatory cell death—as a key player in both COPD and aging. Our preliminary data show increased activation of a necroptosis marker, RIP3, in aged lung tissues, and greater sensitivity of aged lung cells to cigarette smoke-induced cell death. We propose that aging accelerates necroptosis in response to cigarette smoke, making older individuals more susceptible to COPD. This project aims to understand how targeting RIP3-mediated necroptosis could reduce inflammation and lung damage, offering a potential new therapy to prevent or slow COPD progression in elderly smokers.
Amount: $989,400
Start date: 2025-07-01
Investigators: Dongshi Chen, Dongshi Chen
Institution: University of Southern California
Funded outputs count: 0
Funder award ID: g9p3hr
OpenAlex ID: G2250390884