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糖尿病性心肌病相关炎症中Toll样受体和炎性小体复合物的激活

Activation of toll-like receptors and inflammasome complexes in the diabetic cardiomyopathy-associated inflammation.

作者信息

Fuentes-Antrás J, Ioan A M, Tuñón J, Egido J, Lorenzo O

机构信息

Cardiovascular Research Laboratory, IIS-Fundación Jiménez Díaz, Autónoma University, Avenida Reyes Católicos 2, 28040 Madrid, Spain.

Cardiovascular Research Laboratory, IIS-Fundación Jiménez Díaz, Autónoma University, Avenida Reyes Católicos 2, 28040 Madrid, Spain ; Spanish Biomedical Research Centre in Diabetes and Associated Metabolic Disorders (CIBERDEM) Network, Avenida Reyes Católicos 2, 28040 Madrid, Spain.

出版信息

Int J Endocrinol. 2014;2014:847827. doi: 10.1155/2014/847827. Epub 2014 Mar 12.

DOI:10.1155/2014/847827
PMID:24744784
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3972909/
Abstract

Diabetic cardiomyopathy is defined as a ventricular dysfunction initiated by alterations in cardiac energy substrates in the absence of coronary artery disease and hypertension. Hyperglycemia, hyperlipidemia, and insulin resistance are major inducers of the chronic low-grade inflammatory state that characterizes the diabetic heart. Cardiac Toll-like receptors and inflammasome complexes may be key inducers for inflammation probably through NF-κB activation and ROS overproduction. However, metabolic dysregulated factors such as peroxisome proliferator-activated receptors and sirtuins may serve as therapeutic targets to control this response by mitigating both Toll-like receptors and inflammasome signaling.

摘要

糖尿病性心肌病被定义为在没有冠状动脉疾病和高血压的情况下,由心脏能量底物改变引发的心室功能障碍。高血糖、高血脂和胰岛素抵抗是糖尿病心脏特征性慢性低度炎症状态的主要诱导因素。心脏Toll样受体和炎性小体复合物可能是炎症的关键诱导因素,可能是通过激活NF-κB和过量产生活性氧。然而,过氧化物酶体增殖物激活受体和沉默调节蛋白等代谢失调因子可能作为治疗靶点,通过减轻Toll样受体和炎性小体信号传导来控制这种反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a362/3972909/1473ebe6fdaa/IJE2014-847827.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a362/3972909/d9eedfe75777/IJE2014-847827.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a362/3972909/1473ebe6fdaa/IJE2014-847827.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a362/3972909/d9eedfe75777/IJE2014-847827.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a362/3972909/1473ebe6fdaa/IJE2014-847827.002.jpg

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