Hypoxanthine Promotes Pulmonary Vascular Remodeling and Adenosine Deaminase Is a Therapeutic Target for Pulmonary Hypertension

Jun-Zhuo Shi, Yong-Jian Zhu, Meng-Jie Zhang, Yi Yan, Lu-Ling Zhao, Hong-Da Zhang, Yan Liu, Wen-Hui Wu, Zhe Cheng, Chun-Guang Qiu, Jie-Jian Kou, Yun-Feng Zhou, Xiao-Bin Pang, Ji-Wang Chen, Xin-Mei Xie, Yang-Yang He, Zhi-Cheng Jing
Huaihe Hospital and Henan University. First Affiliated Hospital of Zhengzhou University. Shanghai Children’s Medical Center, National Children’s Medical Center and Shanghai Jiao Tong University School of Medicine. Chinese Academy of Medical Sciences and Peking Union Medical College. Shanghai Pulmonary Hospital and Tongji University. University of Illinois at Chicago. Guangdong Provincial People’s Hospital and Southern Medical University.
China znc United States

Journal of the American College of Cardiology Basic to Translational Science
JACC Basic Transl Sci 2025; 10:
DOI: 10.1016/j.jacbts.2025.03.005

Abstract
Uric acid metabolism is implicated in the pathogenesis of pulmonary arterial hypertension, wherein the key metabolite hypoxanthine exhibits elevated levels, thereby promoting pulmonary vascular remodeling through facilitation of cell proliferation and migration as well as regulation of adenosine triphosphate binding cassette transport signaling pathway. Consequently, therapeutic interventions targeting hypoxanthine synthesis may hold promise for the management of pulmonary arterial hypertension.

Category
Vascular Cell Biology and Mechanisms of Pulmonary Vascular Disease
Animal Models of Pulmonary Vascular Disease and Therapy
Pulmonary Vascular Pathology

Age Focus: No Age-Related Focus

Fresh or Filed Publication: Fresh (PHresh). Less than 1-2 years since publication

Article Access
Free PDF File or Full Text Article Available Through PubMed or DOI: Yes

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