Division of Surgery & Interventional Science, University College London, Royal Free Campus, London NW3 2QG, UK.
Cardiol Res Pract. 2012;2012:121237. doi: 10.1155/2012/121237. Epub 2012 Feb 7.
Toll-like receptors (TLRs) are key receptors of the innate immune system which are expressed on immune and nonimmune cells. They are activated by both pathogen-associated molecular patterns and endogenous ligands. Activation of TLRs culminates in the release of proinflammatory cytokines, chemokines, and apoptosis. Ischaemia and ischaemia/reperfusion (I/R) injury are associated with significant inflammation and tissue damage. There is emerging evidence to suggest that TLRs are involved in mediating ischaemia-induced damage in several organs. Critical limb ischaemia (CLI) is the most severe form of peripheral arterial disease (PAD) and is associated with skeletal muscle damage and tissue loss; however its pathophysiology is poorly understood. This paper will underline the evidence implicating TLRs in the pathophysiology of cerebral, renal, hepatic, myocardial, and skeletal muscle ischaemia and I/R injury and discuss preliminary data that alludes to the potential role of TLRs in the pathophysiology of skeletal muscle damage in CLI.
Toll 样受体（TLRs）是先天免疫系统的关键受体，在免疫和非免疫细胞上表达。它们被病原体相关分子模式和内源性配体激活。TLRs 的激活最终导致促炎细胞因子、趋化因子和细胞凋亡的释放。缺血和缺血/再灌注（I/R）损伤与显著的炎症和组织损伤有关。有新的证据表明，TLRs 参与介导几种器官的缺血诱导损伤。严重肢体缺血（CLI）是外周动脉疾病（PAD）最严重的形式，与骨骼肌损伤和组织丧失有关；然而，其病理生理学尚不清楚。本文将强调 TLRs 在脑、肾、肝、心肌和骨骼肌缺血和 I/R 损伤的病理生理学中的作用，并讨论暗示 TLRs 在 CLI 中骨骼肌损伤的病理生理学中的潜在作用的初步数据。
