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肌腱损伤中的血脂异常:低密度脂蛋白的编年史。

Hyperlipidemia in tendon injury: chronicles of low-density lipoproteins.

机构信息

Department of Translational Research, Western University of Health Sciences, Pomona, CA, 91766, USA.

出版信息

Cell Tissue Res. 2023 May;392(2):431-442. doi: 10.1007/s00441-023-03748-8. Epub 2023 Feb 4.

Abstract

Hyperlipidemia impacts millions of people globally and has been the major risk factor for developing atherosclerosis and cardiovascular disease. Interestingly, hyperlipidemic subjects exhibit increased incidence of rotator cuff tendon injury (RCTI) and disorganization of tendon matrix. Low-density lipoproteins (LDL) and its oxidized form (ox-LDL) play a crucial role in hyperlipidemia-driven pro-inflammatory responses in multiple tissues including the tendon. The signaling of oxLDL upregulates the inflammatory cytokines, chemokines, adhesion molecules, and the activation of monocytes/macrophages/resident tendon cells and matrix metalloproteinases impairing the tendon homeostasis resulting in the alteration of extracellular matrix. In addition, the hyperlipidemia-driven immune response and subsequent oxidative stress promote degenerative responses in the tendon tissue. However, the pathological mechanisms underlying the occurrence of RCTI in hyperlipidemia and the effect of ox-LDL in tendon matrix are currently unknown. The present review focuses on the implications and perspectives of LDL/oxLDL on the increased incidence of RCTI.

摘要

高脂血症影响着全球数百万人,是导致动脉粥样硬化和心血管疾病的主要危险因素。有趣的是,高脂血症患者的肩袖肌腱损伤 (RCTI) 和肌腱基质紊乱的发生率增加。低密度脂蛋白 (LDL) 及其氧化形式 (ox-LDL) 在包括肌腱在内的多种组织中的高脂血症驱动的促炎反应中发挥关键作用。oxLDL 的信号转导上调了炎症细胞因子、趋化因子、黏附分子以及单核细胞/巨噬细胞/固有肌腱细胞的激活,破坏了肌腱的动态平衡,导致细胞外基质的改变。此外,高脂血症驱动的免疫反应和随后的氧化应激促进了肌腱组织的退行性反应。然而,目前尚不清楚高脂血症中 RCTI 发生的病理机制以及 ox-LDL 在肌腱基质中的作用。本综述重点探讨了 LDL/oxLDL 对 RCTI 发生率增加的意义和观点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e977/10172214/13bd18cadd01/441_2023_3748_Fig1_HTML.jpg

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