Year: 2022
Type: article
Abstract: Kawasaki disease (KD) is an acute autoimmune vascular disease featured with a long stage of febrile. It predominantly afflicts children under 5 years old and causes an increased risk of cardiovascular combinations. The onset and progression of KD are impacted by many aspects, including genetic susceptibility, infection, and immunity. In recent years, many studies revealed that miRNAs, a novel class of small non-coding RNAs, may play an indispensable role in the development of KD via differential expression and participation in the central pathogenesis of KD comprise of the modulation of immunity, inflammatory response and vascular dysregulation. Although specific diagnose criteria remains unclear up to date, accumulating clinical evidence indicated that miRNAs, as small molecules, could serve as potential diagnostic biomarkers and exhibit extraordinary specificity and sensitivity. Besides, miRNAs have gained attention in affecting therapies for Kawasaki disease and providing new insights into personalized treatment. Through consanguineous coordination with classical therapies, miRNAs could overcome the inevitable drug-resistance and poor prognosis problem in a novel point of view. In this review, we systematically reviewed the existing literature and summarized those findings to analyze the latest mechanism to explore the role of miRNAs in the treatment of KD from basic and clinical aspects retrospectively. Our discussion helps to better understand the pathogenesis of KD and may offer profound inspiration on KD diagnosis, treatment, and prognosis.
Source: Frontiers in Immunology
Authors: Yiyi Xiong, Jiawei Xu, Deju Zhang, Shuqin Wu, Zhangwang Li, Jing Zhang, Zhongbin Xia, Panpan Xia, Cai Xia, Xiaoyi Tang, Xiao Liu, Jianping Liu, Peng Yu
Language: English
Subfield: Surgery
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $2,950
Awards: G1068008773, G1419466742, G1980811909, G1990105307, G2334107167, G3460153528, G3511792118, G3591007811, G3596026476, G3659090986, G3821092586, G4596022524, G5259586241, G5298038910, AMPK参与程序性坏死及其作为心肌缺血再灌注损伤防护靶点的研究, 基于Parkin介导的线粒体自噬探讨七氟烷后处理对糖尿病心肌缺血再灌注损伤的作用机制, G8137521272, G872522648, G8870341198, G996049370
OpenAlex ID: W4307269791