Chinese Medical Sciences Journal ›› 2017, Vol. 32 ›› Issue (4): 253-259.doi: 10.24920/J1001-9294.2017.037

• Review • Previous Articles     Next Articles

Role of ROS/Kv/HIF Axis in the Development of Hypoxia-Induced Pulmonary Hypertension

Wu Wen1, Li Yan2, Xu Dunquan3, *()   

  1. 1 Department of Ultrasound, General Hospital of the Army, Beijing 100007, China
    2. Medical Examination Center, General Hospital of the Army, Beijing 100007, China
    3 Clinical Laboratory, the Xigaze Branch of Xinqiao Hospital, the Army Medical University, Xigaze, Tibet 857000, China
  • Received:2016-10-24 Published:2017-12-30 Online:2017-12-30
  • Contact: Xu Dunquan
The author proposed that “ROS/Kv/HIF axis” participate in the process of hypoxia-induced
pulmonary vasoconstriction and vascular remodeling, and play an important initial role in the development of hypoxia-induced pulmonary hypertension.

Hypoxic pulmonary hypertension (HPH) is a common complication in patients with chronic obstructive pulmonary disease (COPD), sleep-disordered breathing, or dwellers in high altitude. The exact mechanisms underlying the development of HPH still remain unclear. Reactive oxygen species (ROS), hypoxia inducible factors (HIF), and potassium channels (KV) are believed as the main factors during the development of HPH. We propose that the “ROS/Kv/HIF axis” may play an important initiating role in the development of HPH. Being formed under a hypoxic condition, ROS affects the expression and function of HIFs or KV, and consequently triggers multiple downstream signaling pathways and genes expression that participate in promoting pulmonary vasoconstriction and arterial remodeling. Thus, further study determining the initiating role of “ROS/Kv/HIF axis” in the development of HPH could provide theoretic evidences to better understand the underlying mechanisms of HPH, and help identify new potential targets in the treatment of HPH.

Key words: hypoxia-induced pulmonary hypertension, reactive oxygen species, hypoxia inducible factors, potassium channels, vasoconstriction, arterial remodeling

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