Inactivation of carboxyl terminus of Hsc70‐interacting protein prevents hypoxia‐induced pulmonary arterial smooth muscle cells proliferation by reducing intracellular Ca 2+ concentration
Author:
Affiliation:
1. College of Medicine and HealthLishui UniversityLishuiZhejiangPeople’s Republic of China
Funder
PhD Research Startup Fund of Lishui University
Publisher
Wiley
Subject
Pulmonary and Respiratory Medicine
Link
https://onlinelibrary.wiley.com/doi/pdf/10.1177/2045894019875343
Reference42 articles.
1. Hypoxia-Induced Pulmonary Vascular Remodeling
2. Bortezomib alleviates experimental pulmonary hypertension by regulating intracellular calcium homeostasis in PASMCs
3. Cellular and Molecular Basis of Pulmonary Arterial Hypertension
4. Cellular and molecular mechanisms of pulmonary vascular remodeling: role in the development of pulmonary hypertension
5. Chronic Hypoxia–Induced Upregulation of Store-Operated and Receptor-Operated Ca 2+ Channels in Pulmonary Arterial Smooth Muscle Cells
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1. Emodin activates BK channel in vascular smooth muscle cells and relaxes the interlobar renal artery of rat;Biomedicine & Pharmacotherapy;2022-09
2. Evaluation of anisodamine-mediated amelioration of hypoxic injury in brain microvascular endothelial cells;Tropical Journal of Pharmaceutical Research;2022-02-14
3. Carboxyl terminus of Hsc70-interacting protein (CHIP) promotes pulmonary artery smooth muscle cell (PASMC) proliferation via enhancement of intracellular Ca2+ concentration ([Ca2+]i);Experimental Lung Research;2020-09-02
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