| First Author | Meng L | Year | 2016 |
| Journal | Biochem Biophys Res Commun | Volume | 473 |
| Issue | 2 | Pages | 497-502 |
| PubMed ID | 26995086 | Mgi Jnum | J:234815 |
| Mgi Id | MGI:5790910 | Doi | 10.1016/j.bbrc.2016.03.059 |
| Citation | Meng L, et al. (2016) RIP3-dependent necrosis induced inflammation exacerbates atherosclerosis. Biochem Biophys Res Commun 473(2):497-502 |
| abstractText | 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-1alpha production. Injection of anti-IL-1alpha 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. |
