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脑心综合征与糖尿病:糖尿病状态下缺血性脑卒中后的心脏损害。

Cerebral-Cardiac Syndrome and Diabetes: Cardiac Damage After Ischemic Stroke in Diabetic State.

机构信息

Department of Anesthesiology, Zhujiang Hospital of Southern Medical University, Guangzhou, China.

State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China.

出版信息

Front Immunol. 2021 Aug 27;12:737170. doi: 10.3389/fimmu.2021.737170. eCollection 2021.

DOI:10.3389/fimmu.2021.737170
PMID:34512671
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8430028/
Abstract

Cerebral-cardiac syndrome (CCS) refers to cardiac dysfunction following varying brain injuries. Ischemic stroke is strongly evidenced to induce CCS characterizing as arrhythmia, myocardial damage, and heart failure. CCS is attributed to be the second leading cause of death in the post-stroke stage; however, the responsible mechanisms are obscure. Studies indicated the possible mechanisms including insular cortex injury, autonomic imbalance, catecholamine surge, immune response, and systemic inflammation. Of note, the characteristics of the stroke population reveal a common comorbidity with diabetes. The close and causative correlation of diabetes and stroke directs the involvement of diabetes in CCS. Nevertheless, the role of diabetes and its corresponding molecular mechanisms in CCS have not been clarified. Here we conclude the features of CCS and the potential role of diabetes in CCS. Diabetes drives establish a "primed" inflammatory microenvironment and further induces severe systemic inflammation after stroke. The boosted inflammation is suspected to provoke cardiac pathological changes and hence exacerbate CCS. Importantly, as the key element of inflammation, NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome is indicated to play an important role in diabetes, stroke, and the sequential CCS. Overall, we characterize the corresponding role of diabetes in CCS and speculate a link of NLRP3 inflammasome between them.

摘要

脑心综合征(CCS)是指各种脑损伤后继发的心脏功能障碍。缺血性中风强烈证实可诱导 CCS,其特征为心律失常、心肌损伤和心力衰竭。CCS 是中风后阶段的第二大致死原因;然而,其负责的机制尚不清楚。研究表明,可能的机制包括岛叶皮质损伤、自主神经失衡、儿茶酚胺激增、免疫反应和全身炎症。值得注意的是,中风患者的特点显示出与糖尿病的常见共病。糖尿病与中风的密切和因果关系表明糖尿病参与了 CCS。然而,糖尿病及其在 CCS 中的相应分子机制的作用尚未阐明。在这里,我们总结了 CCS 的特征和糖尿病在 CCS 中的潜在作用。糖尿病驱动建立了一个“致敏”的炎症微环境,并在中风后进一步引发严重的全身炎症。炎症的增强被怀疑会引起心脏病理变化,从而加重 CCS。重要的是,作为炎症的关键因素,NOD 样受体富含亮氨酸重复序列 3(NLRP3)炎性小体被认为在糖尿病、中风和随后的 CCS 中发挥重要作用。总的来说,我们描述了糖尿病在 CCS 中的相应作用,并推测它们之间存在 NLRP3 炎性小体的联系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/669b/8430028/4bdda0cb02df/fimmu-12-737170-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/669b/8430028/2779bb21f02c/fimmu-12-737170-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/669b/8430028/3f37550b45fd/fimmu-12-737170-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/669b/8430028/4bdda0cb02df/fimmu-12-737170-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/669b/8430028/2779bb21f02c/fimmu-12-737170-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/669b/8430028/3f37550b45fd/fimmu-12-737170-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/669b/8430028/4bdda0cb02df/fimmu-12-737170-g003.jpg

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