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基质金属蛋白酶在 ECM 重塑和斑块易损性中的作用。

Role of oncostatin-M in ECM remodeling and plaque vulnerability.

机构信息

Department of Translational Research, College of Osteopathic Medicine of the Pacific, Western University of Health Sciences, 309 E. Second Street, Pomona, CA, 91766-1854, USA.

出版信息

Mol Cell Biochem. 2023 Nov;478(11):2451-2460. doi: 10.1007/s11010-023-04673-8. Epub 2023 Mar 1.

DOI:10.1007/s11010-023-04673-8
PMID:36856919
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10579161/
Abstract

Atherosclerosis is a multifactorial inflammatory disease characterized by the development of plaque formation leading to occlusion of the vessel and hypoxia of the tissue supplied by the vessel. Chronic inflammation and altered collagen expression render stable plaque to unstable and increase plaque vulnerability. Thinned and weakened fibrous cap results in plaque rupture and formation of thrombosis and emboli formation leading to acute ischemic events such as stroke and myocardial infarction. Inflammatory mediators including TREM-1, TLRs, MMPs, and immune cells play a critical role in plaque vulnerability. Among the other inflammatory mediators, oncostatin-M (OSM), a pro-inflammatory cytokine, play an important role in the development and progression of atherosclerosis, however, the role of OSM in plaque vulnerability and extracellular matrix remodeling (ECM) is not well understood and studied. Since ECM remodeling plays an important role in atherosclerosis and plaque vulnerability, a detailed investigation on the role of OSM in ECM remodeling and plaque vulnerability is critical. This is important because the role of OSM has been discussed in the context of proliferation of vascular smooth muscle cells and regulation of cytokine expression but the role of OSM is scarcely discussed in relation to ECM remodeling and plaque vulnerability. This review focuses on critically discussing the role of OSM in ECM remodeling and plaque vulnerability.

摘要

动脉粥样硬化是一种多因素炎症性疾病,其特征是斑块形成导致血管阻塞和血管供应的组织缺氧。慢性炎症和胶原蛋白表达改变使稳定斑块不稳定,并增加斑块易损性。纤维帽变薄和变弱导致斑块破裂、血栓形成和栓塞形成,导致急性缺血事件,如中风和心肌梗死。炎症介质,包括 TREM-1、TLRs、MMPs 和免疫细胞,在斑块易损性中发挥关键作用。在其他炎症介质中,促炎细胞因子肿瘤坏死因子样弱诱导剂 1(TREM-1)在动脉粥样硬化的发生和发展中起着重要作用,然而,OSM 在斑块易损性和细胞外基质重塑(ECM)中的作用尚未得到很好的理解和研究。由于 ECM 重塑在动脉粥样硬化和斑块易损性中起着重要作用,因此详细研究 OSM 在 ECM 重塑和斑块易损性中的作用至关重要。这很重要,因为 OSM 的作用已在血管平滑肌细胞增殖和细胞因子表达调节的背景下进行了讨论,但 OSM 在 ECM 重塑和斑块易损性方面的作用却很少被讨论。这篇综述重点讨论了 OSM 在 ECM 重塑和斑块易损性中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7de/10579161/9dafe3229f10/11010_2023_4673_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7de/10579161/f397cceaa32f/11010_2023_4673_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7de/10579161/9dafe3229f10/11010_2023_4673_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7de/10579161/f397cceaa32f/11010_2023_4673_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7de/10579161/9dafe3229f10/11010_2023_4673_Fig2_HTML.jpg

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