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甲硫氨酸亚砜还原酶B2可预防糖尿病的心脏并发症。

Methionine sulfoxide reductase B2 protects against cardiac complications in diabetes mellitus.

作者信息

Lee Seung Hee, Cho Suyeon, Lee Jong Youl, Kim Ji Yeon, Kim Suji, Jeong Myoungho, Hong Jung Yeon, Kim Geun-Young, Lee Seung Woo, Kim Eunmi, Kim Jihwa, Kim Jee Woong, Hwa John, Kim Won-Ho

机构信息

Division of Cardiovascular Disease Research, Department for Chronic Disease Convergence Research, Korea National Institute of Health, Cheongju, Republic of Korea.

Division of Endocrine and Kidney Disease Research, Department for Chronic Disease Convergence Research, Korea National Institute of Health, Cheongju, Republic of Korea.

出版信息

Diabetol Metab Syndr. 2024 Jul 5;16(1):149. doi: 10.1186/s13098-024-01390-0.

DOI:10.1186/s13098-024-01390-0
PMID:38970135
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11225187/
Abstract

Diabetes mellitus (DM) is a progressive, chronic metabolic disorder characterized by high oxidative stress, which can lead to cardiac damage. Methionine sulfoxylation (MetO) of proteins by excessive reactive oxygen species (ROS) can impair the basic functionality of essential cellular proteins, contributing to heart failure. Methionine sulfoxide reductase B2 (MsrB2) can reverse oxidation induced MetO in mitochondrial proteins, so we investigated its role in diabetic cardiomyopathy. We observed that DM-induced heart damage in diabetic mice model is characterized by increased ROS, increased protein MetO with mitochondria structural pathology, and cardiac fibrosis. In addition, MsrB2 was significantly increased in mouse DM cardiomyocytes, supporting the induction of a protective process. Further, MsrB2 directly induces Parkin and LC3 activation (mitophagy markers) in cardiomyocytes. In MsrB2, knockout mice displayed abnormal electrophysiological function, as determined by ECG analysis. Histological analysis confirmed increased cardiac fibrosis and disrupted cardiac tissue in MsrB2 knockout DM mice. We then corroborated our findings in human DM heart samples. Our study demonstrates that increased MsrB2 expression in the heart protects against diabetic cardiomyopathy.

摘要

糖尿病（DM）是一种进行性慢性代谢紊乱，其特征为高氧化应激，可导致心脏损伤。过量活性氧（ROS）使蛋白质发生甲硫氨酸亚砜化（MetO）会损害重要细胞蛋白的基本功能，进而导致心力衰竭。甲硫氨酸亚砜还原酶B2（MsrB2）可逆转线粒体蛋白中由氧化诱导的MetO，因此我们研究了其在糖尿病性心肌病中的作用。我们观察到，糖尿病小鼠模型中糖尿病诱导的心脏损伤表现为ROS增加、蛋白质MetO增加并伴有线粒体结构病变以及心脏纤维化。此外，MsrB2在小鼠糖尿病心肌细胞中显著增加，支持了一种保护过程的诱导。进一步研究发现，MsrB2可直接诱导心肌细胞中Parkin和LC3激活（线粒体自噬标志物）。通过心电图分析确定，MsrB2基因敲除小鼠表现出异常的电生理功能。组织学分析证实，MsrB2基因敲除的糖尿病小鼠心脏纤维化增加且心脏组织遭到破坏。然后，我们在人类糖尿病心脏样本中证实了我们的研究结果。我们的研究表明，心脏中MsrB2表达增加可预防糖尿病性心肌病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bba9/11225187/084a90b3ad03/13098_2024_1390_Fig7_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bba9/11225187/084a90b3ad03/13098_2024_1390_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bba9/11225187/218f19f3c0f3/13098_2024_1390_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bba9/11225187/75e796c87a35/13098_2024_1390_Fig2_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bba9/11225187/22ad886b7b97/13098_2024_1390_Fig5_HTML.jpg
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本文引用的文献

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2024 update in heart failure.2024年心力衰竭治疗进展
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Managing thrombotic risk in patients with diabetes.管理糖尿病患者的血栓风险。
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