title: TLRs are important inflammatory factors in atherosclerosis and may be a therapeutic target.
abstract: Inflammation and immune reactions are implicated in atherogenesis and plaque disruption. The precise triggers for inflammation in atherosclerosis are not fully understood but may include hypercholesterolemia, modified lipoproteins and local or distant infections. TLRs play an important role in the innate and inflammatory signaling responses to microbial agents. Evidence from diverse sources has suggested that TLRs can affect atherosclerosis in multiple ways. Several reports have documented the expression of TLRs in atherosclerotic lesions and suggested that the TLR-NF-kappa B pathway is activated in the lesion, resulting in the transcription of a variety of genes involved in the inflammatory and proliferative responses of cells critical to atherogenesis and ultimately leading to the synthesis and release of antimicrobial peptides and inflammatory cytokines that provide a critical link to adaptive immunity. Moreover, TLR4 expression in macrophages is up-regulated by oxidized LDL, which suggests a potential mechanism for the synergistic effects of hypercholesterolemia and infection in acceleration of atherosclerosis. These findings indicate that TLRs provide additional new insights into the link among lipids, infection/inflammation and atherosclerosis, thus may be effective therapeutic target molecules. We speculate that TLRs are important for the development and progression of atherosclerosis, and hence blocking the expression of TLRs may serve as new targets for antiatherogenic therapy.
authors: School of Medicine, Shandong University, Jinan, Shandong, China.
authors: Yunfang
authors: Y
authors: Liu
authors: Huiming
authors: H
authors: Yu
authors: Yun
authors: Y
authors: Zhang
authors: Yuxia
authors: Y
authors: Zhao
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology; D006801:Humans; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors / Q000502:physiology*; D008955:Models, Cardiovascular; D015398:Signal Transduction; D051193:Toll-Like Receptors / Q000037:antagonists & inhibitors / Q000502:physiology*
chemical_list: D018836:Inflammation Mediators; D051193:Toll-Like Receptors