1. Toll-like receptor 3 involvement in vascular function.
- Author
-
Matsumoto T, Nagano T, Taguchi K, Kobayashi T, and Tanaka-Totoribe N
- Subjects
- Humans, Animals, Endothelial Cells metabolism, Endothelial Cells drug effects, Poly I-C pharmacology, Signal Transduction, Toll-Like Receptor 3 metabolism, Toll-Like Receptor 3 agonists, Muscle, Smooth, Vascular metabolism, Muscle, Smooth, Vascular drug effects
- Abstract
Maintaining endothelial cell (EC) and vascular smooth muscle cell (VSMC) integrity is an important component of human health and disease because both EC and VSMC regulate various functions, including vascular tone control, cellular adhesion, homeostasis and thrombosis regulation, proliferation, and vascular inflammation. Diverse stressors affect functions in both ECs and VSMCs and abnormalities of functions in these cells play a crucial role in cardiovascular disease initiation and progression. Toll-like receptors (TLRs) are important detectors of pathogen-associated molecular patterns derived from various microbes and viruses as well as damage-associated molecular patterns derived from damaged cells and perform innate immune responses. Among TLRs, several studies reveal that TLR3 plays a key role in initiation, development and/or protection of diseases, and an emerging body of evidence indicates that TLR3 presents components of the vasculature, including ECs and VSMCs, and plays a functional role. An agonist of TLR3, polyinosinic-polycytidylic acid [poly (I:C)], affects ECs, including cell death, inflammation, chemoattractant, adhesion, permeability, and hemostasis. Poly (I:C) also affects VSMCs including inflammation, proliferation, and modulation of vascular tone. Moreover, alterations of vascular function induced by certain molecules and/or interventions are exerted through TLR3 signaling. Hence, we present the association between TLR3 and vascular function according to the latest studies., Competing Interests: Declaration of competing interest There are no potential conflicts of interest among the authors regarding the publication of this manuscript., (Copyright © 2024 Elsevier B.V. All rights reserved.)
- Published
- 2024
- Full Text
- View/download PDF