Mitochondrial TOM70 in Hyperoxia‐induced Acute Lung Injury
Abstract
Hyperoxia‐induced acute lung injury (HALI) leads to respiratory failure and mitochondrial dysfunction is a critical mediator of HALI. We previously reported Toll‐Like Receptor (TLR)4 prevents oxidant‐induced ALI by maintaining mitochondrial bioenergetics in mammalian lung endothelium (Ec). Translocase of Outer Mitochondrial Membrane (TOM) have recently been identified to play important roles in mitochondrial quality control, primarily in yeast [1]. TOM70 is an essential subunit of TOM and mediates uptake of newly synthesized proteins to mitochondria as well has putative anti‐oxidant and anti‐apoptotic properties. TOM70 appeared to parallel many of the cytoprotective signaling properties of TLR4 [2‐4]. Therefore, our hypothesis is TLR4 regulates TOM70 expression and TOM70 has mitochondrial and lung protective functions in HALI.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- May 01, 2022
- Source ID
- 10.1096/fasebj.2022.36.s1.l7461
Entities
People
- Chuankai Zhou
- Elias Coutavas
- Patty J Lee
- So‐jin Kim
Organizations
- Buck Institute for Research on Aging
- Duke University
- National Heart, Lung, and Blood Institute
- National Institutes of Health
- United States Department of Defense