FGF21 attenuates hypoxia‑induced dysfunction and apoptosis in HPAECs through alleviating endoplasmic reticulum stress

International Journal of Molecular Medicine
Ali ChenXiaoying Huang

Abstract

Vascular endothelial apoptosis and dysfunction have a crucial role in triggering pathological vascular remodeling of hypoxia‑induced pulmonary arterial hypertension (PAH). Fibroblast growth factor (FGF)21, an endocrine regulator, has recently been reported to protect cardiac endothelial cells from damage and suppress inflammatory responses. In addition, FGF21 is reported to be involved in endoplasmic reticulum stress (ERS). Previous studies have suggested that ERS participates in the development of PAH, and attenuation of ERS could be an effective therapeutic strategy for the protection of pulmonary arteries. However, whether FGF21 has a protective function via suppression of ERS in pulmonary arterial endothelial cells in hypoxia remains unclear. The present study aimed to explore whether FGF21 could reduce the hypoxia‑induced apoptosis of human pulmonary arterial endothelial cells (HPAECs) and prevent endothelial dysfunction via the inhibition of ERS. HPAECs were divided into six groups: Normoxia, hypoxia, hypoxia plus FGF21, hypoxia plus salubrinal (an ERS inhibitor), hypoxia plus tunicamycin (an ERS agonist), and hypoxia plus tunicamycin plus FGF21. The endoplasmic reticulum ultrastructure in HPAECs was assessed by transmiss...Continue Reading

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Citations

Feb 5, 2021·International Journal of Molecular Sciences·Aimilia Eirini PapathanasiouHelen Christou
Jul 24, 2021·Diabetes, Metabolic Syndrome and Obesity : Targets and Therapy·Wei LinZhenlang Lin

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