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2型糖尿病中的红细胞通过精氨酸酶依赖性调节一氧化氮合酶和活性氧来损害心脏缺血后的恢复。

Red Blood Cells in Type 2 Diabetes Impair Cardiac Post-Ischemic Recovery Through an Arginase-Dependent Modulation of Nitric Oxide Synthase and Reactive Oxygen Species.

作者信息

Yang Jiangning, Zheng Xiaowei, Mahdi Ali, Zhou Zhichao, Tratsiakovich Yahor, Jiao Tong, Kiss Attila, Kövamees Oskar, Alvarsson Michael, Catrina Sergiu-Bogdan, Lundberg Jon O, Brismar Kerstin, Pernow John

机构信息

Division of Cardiology, Department of Medicine, Karolinska Institutet, Karolinska University Hospital, Stockhom, Sweden.

Division of Endocrinology and Diabetology, Department of Molecular Medicine and Surgery, Karolinska Institutet, Karolinska University Hospital, Stockhom, Sweden.

出版信息

JACC Basic Transl Sci. 2018 Jul 18;3(4):450-463. doi: 10.1016/j.jacbts.2018.03.006. eCollection 2018 Aug.

DOI:10.1016/j.jacbts.2018.03.006
PMID:30175269
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6115643/
Abstract

This study tested the hypothesis that red blood cell (RBC) arginase represents a potential therapeutic target in ischemia-reperfusion in type 2 diabetes. Post-ischemic cardiac recovery was impaired in hearts from db/db mice compared with wild-type hearts. RBCs from mice and patients with type 2 diabetes attenuated post-ischemic cardiac recovery of nondiabetic hearts. This impaired cardiac recovery was reversed by inhibition of RBCs arginase or nitric oxide synthase. The results suggest that RBCs from type 2 diabetics impair cardiac tolerance to ischemia-reperfusion via a pathway involving arginase activity and nitric oxide synthase-dependent oxidative stress.

摘要

本研究检验了以下假设

红细胞精氨酸酶是2型糖尿病缺血再灌注中的一个潜在治疗靶点。与野生型心脏相比，db/db小鼠心脏的缺血后心脏恢复受损。来自2型糖尿病小鼠和患者的红细胞减弱了非糖尿病心脏的缺血后心脏恢复。抑制红细胞精氨酸酶或一氧化氮合酶可逆转这种受损的心脏恢复。结果表明，2型糖尿病患者的红细胞通过涉及精氨酸酶活性和一氧化氮合酶依赖性氧化应激的途径损害心脏对缺血再灌注的耐受性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b112/6115643/50a00e0fca82/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b112/6115643/952d94cacb2b/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b112/6115643/d0b14eeda282/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b112/6115643/713a6188dbc3/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b112/6115643/1fab556e1744/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b112/6115643/d499f4cc2b14/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b112/6115643/271b52296348/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b112/6115643/b459f6281a1c/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b112/6115643/bca1d3ec7ce1/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b112/6115643/50a00e0fca82/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b112/6115643/952d94cacb2b/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b112/6115643/d0b14eeda282/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b112/6115643/713a6188dbc3/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b112/6115643/1fab556e1744/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b112/6115643/d499f4cc2b14/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b112/6115643/271b52296348/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b112/6115643/b459f6281a1c/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b112/6115643/bca1d3ec7ce1/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b112/6115643/50a00e0fca82/gr8.jpg

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Effect of arginase inhibition on ischemia-reperfusion injury in patients with coronary artery disease with and without diabetes mellitus.
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Front Nutr. 2025 Jul 9;12:1607386. doi: 10.3389/fnut.2025.1607386. eCollection 2025.
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