Critical role of mitochondrial dynamics in chronic respiratory diseases and new therapeutic directions.
10.1097/CM9.0000000000003704
- Author:
Xiaomei WANG
1
;
Ziming ZHU
2
;
Haocheng JIA
3
;
Xueyi LU
3
;
Yingze ZHANG
4
;
Yingxin ZHU
3
;
Jinzheng WANG
2
;
Yanfang WANG
5
;
Rubin TAN
6
;
Jinxiang YUAN
7
Author Information
1. College of Basic Medical, Jining Medical University, Jining, Shandong 272067, China.
2. College of Second Clinical Medicine, Jining Medical University, Jining, Shandong 272067,China.
3. College of Clinical Medicine, Jining Medical University, Jining, Shandong 272067,China.
4. College of Dental Medicine, Jining Medical University, Jining, Shandong 272067,China.
5. Lin He's Academician Workstation of New Medicine and Clinical Translation, Jining Medical University, Jining, Shandong 272067, China.
6. College of Basic Medical, Xuzhou Medical University, Xuzhou, Jiangsu 221004,China.
7. State Key Laboratory of Animal Biotech Breeding, Institute of Animal Science, Chinese Academy of Agricultural Sciences, Beijing 100193, China.
- Publication Type:Review
- Keywords:
Chronic obstructive pulmonary disease;
Chronic respiratory system diseases;
Mitochondrial dynamics;
New therapeutic directions;
Pulmonary hypertension
- MeSH:
Humans;
Mitochondrial Dynamics/physiology*;
Pulmonary Disease, Chronic Obstructive/metabolism*;
Hypertension, Pulmonary/metabolism*;
Mitochondria/metabolism*;
Animals
- From:
Chinese Medical Journal
2025;138(15):1783-1793
- CountryChina
- Language:English
-
Abstract:
Chronic obstructive pulmonary disease (COPD) and pulmonary hypertension (PH) are both chronic progressive respiratory diseases that cannot be completely cured. COPD is characterized by irreversible airflow limitation, chronic airway inflammation, and gradual decline in lung function, whereas PH is characterized by pulmonary vasoconstriction, remodeling, and infiltration of inflammatory cells. These diseases have similar pathological features, such as vascular hyperplasia, arteriolar contraction, and inflammatory infiltration. Despite these well-documented observations, the exact mechanisms underlying the occurrence and development of COPD and PH remain unclear. Evidence that mitochondrial dynamics imbalance is one major factor in the development of COPD and PH. Mitochondrial dynamics is precisely regulated by mitochondrial fusion proteins and fission proteins. When mitochondrial dynamics equilibrium is disrupted, it causes mitochondrial and even cell morphological dysfunction. Mitochondrial dynamics participates in various pathological processes for heart and lung disease. Mitochondrial dynamics may be different in the early and late stages of COPD and PH. In the early stages of the disease, mitochondrial fusion increases, inhibiting fission, and thereby compensatorily increasing adenosine triphosphate (ATP) production. With the development of the disease, mitochondria decompensation causes excessive fission. Mitochondrial dynamics is involved in the development of COPD and PH in a spatiotemporal manner. Based on this understanding, treatment strategies for mitochondrial dynamics abnormalities may be different at different stages of COPD and PH disease. This article will provide new ideas for the potential treatment of related diseases.
