血管内皮蛋白酪氨酸磷酸酶在糖尿病中对一氧化氮合酶功能的作用：从分子生物学到临床
The role of vascular endothelial protein tyrosine phosphatase on nitric oxide synthase function in diabetes: from molecular biology to the clinic.
作者信息
Justo Alberto Fernando Oliveira, Afonso Pedro Paulo Luciano
机构信息
Department of Medicine, Federal University of São Paulo - UNIFESP, São Paulo, São Paulo, Brazil.
Hospital Municipal do Campo Limpo, São Paulo, São Paulo, Brazil.
出版信息
J Cell Commun Signal. 2021 Sep;15(3):467-471. doi: 10.1007/s12079-021-00611-9. Epub 2021 Mar 8.
Abstract
Endothelial nitric oxide synthase (eNOS) and receptor-type vascular endothelial protein tyrosine phosphatase (VE-PTP) are one of the majors signaling pathways related to endothelial health in diabetes. Several reports have shown that the inhibition of VE-PTP can lead the nitric oxide production, although repeated studies showed that VE-PTP regulated the eNOS exclusive at Ser1177 in indirect-manner. A recent, exciting paper (Siragusa et al. in Cardiovasc Res, 2020. https://doi.org/10.1093/cvr/cvaa213 ), showing that VE-PTP regulates eNOS in a direct-manner, dephosphorylating eNOS at Tyr81 and indirect at Ser1177 and the effects of a VE-PTP inhibitor, AKB-9778, in the blood pressure from diabetic patients.
摘要
内皮型一氧化氮合酶（eNOS）和受体型血管内皮蛋白酪氨酸磷酸酶（VE-PTP）是糖尿病中与内皮健康相关的主要信号通路之一。多项报告表明，抑制VE-PTP可导致一氧化氮生成，尽管反复研究表明VE-PTP以间接方式仅在Ser1177位点调节eNOS。最近有一篇令人兴奋的论文（Siragusa等人，发表于《心血管研究》，2020年。https://doi.org/10.1093/cvr/cvaa213 ）表明，VE-PTP以直接方式调节eNOS，使eNOS的Tyr81位点去磷酸化，并间接使Ser1177位点去磷酸化，以及VE-PTP抑制剂AKB-9778对糖尿病患者血压的影响。
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