Novel Role for Tranilast in Regulating NLRP3 Ubiquitination, Vascular Inflammation, and Atherosclerosis

• Published in: Journal of the American Heart Association Vol. 9; no. 12; p. e015513
• Main Authors: Chen, Suwen, Wang, Yadong, Pan, Yamu, Liu, Yao, Zheng, Shuang, Ding, Ke, Mu, Kaiyu, Yuan, Ye, Li, Zhaoyang, Song, Hongxian, Jin, Ying, Fu, Jian
• Format: Journal Article
• Language: English
• Published: England John Wiley and Sons Inc 16.06.2020; Wiley
• Subjects: Animals; Anti-Inflammatory Agents, Non-Steroidal - pharmacology; atherosclerosis; Atherosclerosis - metabolism; Atherosclerosis - pathology; Atherosclerosis - prevention & control; Disease Models, Animal; HEK293 Cells; Humans; inflammasome; Inflammasomes - metabolism; Inflammation Mediators - metabolism; Interleukin-1beta - metabolism; Macrophages - drug effects; Macrophages - metabolism; Mice, Knockout, ApoE; NLR Family, Pyrin Domain-Containing 3 Protein - genetics; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism; NLRP3 ubiquitination; Original Research; ortho-Aminobenzoates - pharmacology; Plaque, Atherosclerotic; Receptors, LDL - deficiency; Receptors, LDL - genetics; tranilast; Ubiquitination; vascular inflammation; Vasculitis - metabolism; Vasculitis - pathology; Vasculitis - prevention & control; atherosclerosis; tranilast; vascular inflammation; inflammasome; NLRP3 ubiquitination

Background Aberrant activation of the NLRP3 (nucleotide-binding oligomerization domain, leucine-rich repeat-containing receptor family pyrin domain-containing 3) inflammasome is thought to play a causative role in atherosclerosis. NLRP3 is kept in an inactive ubiquitinated state to avoid unwanted NL...