Mitochondrial ribosomal stress in lung diseases
Abstract
Mitochondria are involved in a variety of critical cellular functions, and their impairment drives cell injury. The mitochondrial ribosome (mitoribosome) is responsible for the protein synthesis of mitochondrial DNA-encoded genes. These proteins are involved in oxidative phosphorylation, respiration, and ATP production required in the cell. Mitoribosome components originate from both mitochondrial and nuclear genomes. Their dysfunction can be caused by impaired mitochondrial protein synthesis or mitoribosome misassembly, leading to a decline in mitochondrial translation. This decrease can trigger mitochondrial ribosomal stress and contribute to pulmonary cell injury, death, and diseases. This review focuses on the contribution of the impaired mitoribosome structural components and function to respiratory disease pathophysiology. We present recent findings in the fields of lung cancer, chronic obstructive pulmonary disease, interstitial lung disease, and asthma. We also include reports on the mitoribosome dysfunction in pulmonary hypertension, high-altitude pulmonary edema, and bacterial and viral infections. Studies of the mitoribosome alterations in respiratory diseases can lead to novel therapeutic targets.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Apr 01, 2022
- Source ID
- 10.1152/ajplung.00078.2021
Entities
People
- Beata Kosmider
- Karim Bahmed
- Loukmane Karim
Organizations
- American Lung Association
- National Heart, Lung, and Blood Institute
- National Institute of Environmental Health Sciences
- Temple University
- United States Department of Defense