China State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China; First Clinical School, Guangzhou Medical University, Guangzhou, China.
China State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Heart Lung Circ. 2022 Jul;31(7):e93-e109. doi: 10.1016/j.hlc.2022.02.012. Epub 2022 Mar 30.
Toll-like receptor 3 (TLR3) is an important member of the innate immune response receptor toll-like receptors (TLRs) family, which plays a vital role in regulating immune response, promoting the maturation and differentiation of immune cells, and participating in the response of pro-inflammatory factors. TLR3 is activated by pathogen-associated molecular patterns and damage-associated molecular patterns, which support the pathophysiology of many diseases related to inflammation. An increasing number of studies have confirmed that TLR3, as a crucial medium of innate immunity, participates in the occurrence and development of cardiovascular diseases (CVDs) by regulating the transcription and translation of various cytokines, thus affecting the structure and physiological function of resident cells in the cardiovascular system, including vascular endothelial cells, vascular smooth muscle cells, cardiomyocytes, fibroblasts and macrophages. The dysfunction and structural damage of vascular endothelial cells and proliferation of vascular smooth muscle cells are the key factors in the occurrence of vascular diseases such as pulmonary arterial hypertension, atherosclerosis, myocardial hypertrophy, myocardial infarction, ischaemia/reperfusion injury, and heart failure. Meanwhile, cardiomyocytes, fibroblasts, and macrophages are involved in the development of CVDs. Therefore, the purpose of this review was to explore the latest research published on TLR3 in CVDs and discuss current understanding of potential mechanisms by which TLR3 contributes to CVDs. Even though TLR3 is a developing area, it has strong treatment potential as an immunomodulator and deserves further study for clinical translation.
Toll 样受体 3（TLR3）是先天免疫反应 Toll 样受体（TLRs）家族的重要成员，在调节免疫反应、促进免疫细胞的成熟和分化以及参与前炎性因子的反应中起着至关重要的作用。TLR3 被病原体相关分子模式和损伤相关分子模式激活，这支持了许多与炎症相关的疾病的病理生理学。越来越多的研究证实，TLR3 作为先天免疫的重要介质，通过调节各种细胞因子的转录和翻译，参与心血管疾病（CVDs）的发生和发展，从而影响心血管系统中驻留细胞的结构和生理功能，包括血管内皮细胞、血管平滑肌细胞、心肌细胞、成纤维细胞和巨噬细胞。血管内皮细胞功能障碍和结构损伤以及血管平滑肌细胞增殖是肺动脉高压、动脉粥样硬化、心肌肥大、心肌梗死、缺血/再灌注损伤和心力衰竭等血管疾病发生的关键因素。同时，心肌细胞、成纤维细胞和巨噬细胞也参与了 CVD 的发生。因此，本综述的目的是探讨 TLR3 在 CVDs 中的最新研究进展，并讨论目前对 TLR3 促进 CVDs 发生的潜在机制的理解。尽管 TLR3 是一个正在发展的领域，但作为一种免疫调节剂，它具有很强的治疗潜力，值得进一步研究以实现临床转化。
