Research progress on hypoxia-induced imbalance of calcium homeostasis in pulmonary artery smooth muscle cells and its treatment
- Author:
Xiang-Yun GAI
1
;
En-Qi ZHAO
1
;
Jin-Yu WANG
1
;
Yue-Fu ZHAO
1
;
Yan-Feng HE
1
;
Peng-Cheng LIN
1
;
Xiang-Yun GAI
2
;
En-Qi ZHAO
2
;
Jin-Yu WANG
2
;
Yue-Fu ZHAO
2
;
Yan-Feng HE
2
;
Peng-Cheng LIN
2
Author Information
- Publication Type:Journal Article
- Keywords: calcium homeostasis; hypoxia; hypoxic pulmonary hypertension; hypoxic pulmonary vascular remodeling; hypoxic pulmonary vasoconstriction; pulmonary artery smooth muscle cells
- From: Chinese Pharmacological Bulletin 2022;38(4):492-496
- CountryChina
- Language:Chinese
- Abstract: Chronic hypoxic lung diseases are major causes of disability and mortality worldwide, which are typically aggravated by hypoxic pulmonary hypertension.The pathogenesis of hypoxic pulmonary hypertension is complex, and its mechanism has not been fully elucidated.The previous studies have shown abnormally elevated levels of free Ca + in the cytoplasm of pulmonary artery smooth muscle cells to be the predominant drivers of pulmonary hypertension , causing continuous contraction and remodeling of the pulmonary vessels.This article briefly summarizes the mechanism of hypoxia-induced imbalance in calcium homeostasis in pulmonary artery smooth muscle cells, together with its related drug research, based on the existing literature.Hypoxia induces an imbalance in calcium homeostasis in pulmonary artery smooth muscle cells by regulating hypoxia-inducible factor-1, K+ , store-operated calcium channel, receptor-operated calcium channel, the Ca +-sensing myosin contractile mechanism by binding to calmodulin, leading to pulmonary vasoconstriction.Ca + can also activate PKC/ MAPKs and PI3K/Akt/mTOR pathways, leading to pulmonary vascular remodeling.
