title: RIP3-dependent necrosis induced inflammation exacerbates atherosclerosis.
abstract: Atherothrombotic vascular disease is already the leading cause of mortality worldwide. Atherosclerosis shares features with diseases caused by chronic inflammation. More attention should concentrates on the innate immunity effect atherosclerosis progress. RIP3 (receptor-interacting protein kinase 3) act through the transcription factor named Nr4a3 (Nuclear orphan receptors) to regulate cytokine production. Deletion RIP3 decreases IL-1α production. Injection of anti-IL-1α antibody protects against the progress of atherosclerosis in ApoE -/- mice. RIP3 as a molecular switch in necrosis, controls macrophage necrotic death caused inflammation. Inhibiting necrosis will certainly reduce atherosclerosis through limit inflammation. Necrotic cell death caused systemic inflammation exacerbated cardiovascular disease. Inhibition of necrosis may yield novel therapeutic targets for treatment in years to come.
authors.affiliation: College of Biological Sciences, China Agricultural University, Beijing 100094, China; National Institute of Biological Sciences, Beijing 102206, China. Electronic address: menglingjun@nibs.ac.cn.
authors.forename: Lingjun
authors.initials: L
authors.lastname: Meng
authors.affiliation: Institute for Immunology, Tsinghua University, Beijing 100084, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Jin
authors.affiliation: Institute of Cardiovascular Sciences, Health Science Center, Peking University, Beijing 100191, China.
authors.forename: Yuhui
authors.initials: Y
authors.lastname: Wang
authors.affiliation: National Institute of Biological Sciences, Beijing 102206, China.
authors.forename: Huanwei
authors.initials: H
authors.lastname: Huang
authors.affiliation: National Institute of Biological Sciences, Beijing 102206, China.
authors.forename: Jia
authors.initials: J
authors.lastname: Li
authors.affiliation: National Institute of Biological Sciences, Beijing 102206, China.
authors.forename: Cai
authors.initials: C
authors.lastname: Zhang
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000150:complications* / Q000235:genetics / Q000276:immunology*; D016207:Cytokines / Q000235:genetics / Q000276:immunology; D017353:Gene Deletion; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation; D007249:Inflammation / Q000150:complications* / Q000235:genetics / Q000276:immunology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009336:Necrosis / Q000150:complications* / Q000235:genetics / Q000276:immunology*; D053422:Receptor-Interacting Protein Serine-Threonine Kinases / Q000235:genetics / Q000276:immunology*
chemical_list: D016207:Cytokines; D053422:Receptor-Interacting Protein Serine-Threonine Kinases; C485615:Ripk3 protein, mouse
keywords: IL-1α; Nr4a3; RIP3