Molecular pathogenesis in chronic obstructive pulmonary disease and therapeutic potential by targeting AMP-activated protein kinase.
Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide, which is characterized by a persistent airflow limitation caused by chronic inflammatory responses to noxious particles or gases. Cigarette smoke and environmental pollutions are major etiological factors for causing COPD. It has been shown that cigarette smoking causes abnormal inflammatory responses, cellular senescence, mitochondrial dysfunction and metabolic dysregulation, suggesting their involvement in the development of COPD. Although the medical care and treatment have advanced, there are no effective therapies to stop or reverse lung destruction in COPD/emphysema. AMP-activated protein kinase (AMPK) is a serine threonine kinase with α, β, and γ subunits that are highly conserved through evolution. AMPK has been shown to regulate bioenergetics, inflammatory responses, senescence, and metabolism. This review focused on the updated understanding of molecular pathogenesis of COPD, and highlighted the crucial roles of AMPK in lung abnormalities as well as discussed the potential therapeutics of AMPK activators in preventing and halting the progression of COPD.
The Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.
Zhihui
Z
Zhang
School of Pharmacy, Anhui Medical University Hefei, Anhui, China.
Xiaoyu
X
Cheng
Department of Orthopedics, Warren Alpert Medical School, Brown University/Rhode Island Hospital, Providence, Rhode Island.
Li
L
Yue
The Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.
Wenhui
W
Cui
School of Pharmacy, Anhui Medical University Hefei, Anhui, China.
Wencheng
W
Zhou
The Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.
Jian
J
Gao
Department of Molecular Biology, Cell Biology and Biochemistry, Brown University Warren Alpert Medical School, Providence, Rhode Island.
Hongwei
H
Yao
D055372:AMP-Activated Protein Kinases / Q000378:metabolism*; D000393:Air Pollutants / Q000009:adverse effects*; D016922:Cellular Senescence / Q000187:drug effects*; D006801:Humans; D007249:Inflammation / Q000473:pathology; D008168:Lung / Q000473:pathology*; D008928:Mitochondria / Q000473:pathology; D029424:Pulmonary Disease, Chronic Obstructive / Q000473:pathology* / Q000628:therapy; D012906:Smoke / Q000009:adverse effects*; D012907:Smoking
D000393:Air Pollutants; D012906:Smoke; D055372:AMP-Activated Protein Kinases
AMP-activated protein kinase; cellular senescence; chronic obstructive pulmonary disease; metabolism; mitochondrial dysfunction