索引超出了数组界限。 文章摘要
|本期目录/Table of Contents|

[1]原野,刘洋,徐志云.受体相互作用蛋白激酶1在心血管疾病中的研究进展[J].国际心血管病杂志,2021,06:352-355.
点击复制

受体相互作用蛋白激酶1在心血管疾病中的研究进展(PDF)

《国际心血管病杂志》[ISSN:1006-6977/CN:61-1281/TN]

期数:
2021年06期
页码:
352-355
栏目:
综述
出版日期:
2021-12-01

文章信息/Info

Title:
-
作者:
原野刘洋徐志云
200433 海军军医大学第一附属医院心血管外科(原野,徐志云); 200052 海军军医大学附属海军特色医学中心ICU(刘洋)
Author(s):
-
关键词:
受体相互作用蛋白激酶1 坏死性凋亡 动脉粥样硬化 心肌梗死 腹主动脉瘤
Keywords:
-
分类号:
-
DOI:
10.3969/j.issn.1673-6583.2021.06.009
文献标识码:
-
摘要:
受体相互作用蛋白激酶1(RIPK1)是一种胞内信号蛋白,在炎性反应和坏死性凋亡的信号级联反应中发挥重要的调控作用。该文介绍了RIPK1在心血管疾病中的作用机制,为预防和治疗心血管疾病提供新的思路。
Abstract:
-

参考文献/References

[1] Dhuriya YK, Sharma D. Necroptosis: a regulated inflammatory mode of cell death[J]. J Neuroinflammation, 2018, 15(1):199.
[2] Newton K, Wickliffe KE, Dugger DL, et al. Cleavage of RIPK1 by caspase-8 is crucial for limiting apoptosis and necroptosis[J]. Nature, 2019, 574(7778):428-431.
[3] Khoury MK, Gupta K, Franco SR, et al. Necroptosis in the pathophysiology of disease[J]. Am J Pathol, 2020, 190(2):272-285.
[4] Li X, Zhang M, Huang X, et al. Ubiquitination of RIPK1 regulates its activation mediated by TNFR1 and TLRs signaling in distinct manners[J]. Nat Commun, 2020, 11(1):6364.
[5] Hanson B. Necroptosis: a new way of dying[J]. Cancer Biol Ther, 2016, 17(9):899-910.
[6] Tian F, Yao J, Yan M, et al. 5-aminolevulinic acid-mediated sonodynamic therapy inhibits RIPK1/RIPK3-dependent necroptosis in THP-1-derived foam cells[J]. Sci Rep, 2016, 6:21992.
[7] Herrington W, Lacey B, Sherliker P, et al. Epidemiology of atherosclerosis and the potential to reduce the global burden of atherothrombotic disease[J]. Circ Res, 2016, 118(4):535-546.
[8] Karunakaran D, Nguyen MA, Geoffrion M, et al. RIPK1 expression associates with inflammation in early atherosclerosis in humans and can be therapeutically silenced to reduce NF-kappaB activation and atherogenesis in mice[J]. Circulation, 2021, 143(2):163-177.
[9] Weinlich R, Oberst A, Beere HM, et al. Necroptosis in development, inflammation and disease[J]. Nat Rev Mol Cell Biol, 2017, 18(2):127-136.
[10] Karunakaran D, Geoffrion M, Wei L, et al. Targeting macrophage necroptosis for therapeutic and diagnostic interventions in atherosclerosis[J]. Sci Adv, 2016, 2(7):e1600224.
[11] An S, Qi Y, Zhang Z, et al. Antagonism of receptor interacting protein 1 using necrostatin-1 in oxidized LDL-induced endothelial injury[J]. Biomed Pharmacother, 2018, 108: 1809-1815.
[12] Rasheed A, Robichaud S, Nguyen MA, et al. Loss of MLKL(Mixed Lineage Kinase Domain-Like Protein)decreases necrotic core but increases macrophage lipid accumulation in atherosclerosis[J]. Arterioscler Thromb Vasc Biol, 2020, 40(5):1155-1167.
[13] Liu YR, Xu HM. Protective effect of necrostatin-1 on myocardial tissue in rats with acute myocardial infarction[J]. Genet Mol Res, 2016, 15(2).
[14] Song YF, Zhao L, Wang BC, et al. The circular RNA TLK1 exacerbates myocardial ischemia/reperfusion injury via targeting miR-214/RIPK1 through TNF signaling pathway[J]. Free Radic Biol Med, 2020, 155:69-80.
[15] Cao L, Mu W. Necrostatin-1 and necroptosis inhibition: Pathophysiology and therapeutic implications[J]. Pharmacol Res, 2021, 163:105297.
[16] Oerlemans MI, Liu J, Arslan F, et al. Inhibition of RIP1-dependent necrosis prevents adverse cardiac remodeling after myocardial ischemia-reperfusion in vivo[J]. Basic Res Cardiol, 2012, 107(4):270.
[17] Xiao P, Wang C, Li J, et al. COP9 signalosome suppresses RIPK1-RIPK3-mediated cardiomyocyte necroptosis in mice[J]. Circ Heart Fail, 2020, 13(8):e006996.
[18] Newton K, Dugger DL, Maltzman A, et al. RIPK3 deficiency or catalytically inactive RIPK1 provides greater benefit than MLKL deficiency in mouse models of inflammation and tissue injury[J]. Cell Death Differ, 2016, 23(9):1565-1576.
[19] Zhang DY, Wang BJ, Ma M, et al. MicroRNA-325-3p protects the heart after myocardial infarction by inhibiting RIPK3 and programmed necrosis in mice[J]. BMC Mol Biol, 2019, 20(1):17.
[20] Rodriguez DA, Weinlich R, Brown S, et al. Characterization of RIPK3-mediated phosphorylation of the activation loop of MLKL during necroptosis[J]. Cell Death Differ, 2016, 23(1):76-88.
[21] Xia K, Zhu F, Yang C, et al. Discovery of a potent RIPK3 inhibitor for the amelioration of necroptosis-associated inflammatory injury[J]. Front Cell Dev Biol, 2020, 8:606119.
[22] Liu L, Lalaoui N. 25 years of research put RIPK1 in the clinic[J]. Semin Cell Dev Biol, 2020, 109:86-95.
[23] Liu Z, Fitzgerald M, Meisinger T, et al. CD95-ligand contributes to abdominal aortic aneurysm progression by modulating inflammation[J]. Cardiovasc Res, 2019, 115(4):807-818.
[24] Luo W, Wang Y, Zhang L, et al. Critical role of cytosolic DNA and its sensing adaptor STING in aortic degeneration, dissection, and rupture[J]. Circulation, 2020, 141(1):42-66.
[25] Mifflin L, Ofengeim D, Yuan J. Receptor-interacting protein kinase 1(RIPK1)as a therapeutic target[J]. Nat Rev Drug Discov, 2020, 19(8):553-571.
[26] Zhou T, Wang Q, Phan N, et al. Identification of a novel class of RIP1/RIP3 dual inhibitors that impede cell death and inflammation in mouse abdominal aortic aneurysm models[J]. Cell Death Dis, 2019, 10(3):226.
[27] Wang Q, Zhou T, Liu Z, et al. Inhibition of receptor-interacting protein kinase 1 with necrostatin-1s ameliorates disease progression in elastase-induced mouse abdominal aortic aneurysm model[J]. Sci Rep, 2017, 7:42159.
[28] Zhang Y, Zhang J, Yan R, et al. Receptor-interacting protein kinase 3 promotes platelet activation and thrombosis[J]. Proc Natl Acad Sci U S A, 2017, 114(11):2964-2969.
[29] Saito MS, Lourenco AL, Kang HC, et al. New approaches in tail-bleeding assay in mice: improving an important method for designing new anti-thrombotic agents[J]. Int J Exp Pathol, 2016, 97(3):285-292.
[30] Lule S, Wu L, Sarro-Schwartz A, et al. Cell-specific activation of RIPK1 and MLKL after intracerebral hemorrhage in mice[J]. J Cereb Blood Flow Metab, 2021, 41(7):1623-1633.
[31] Deng XX, Li SS, Sun FY. Necrostatin-1 prevents necroptosis in brains after ischemic stroke via inhibition of RIPK1-mediated RIPK3/MLKL signaling[J]. Aging Dis, 2019, 10(4):807-817.
[32] Nakazawa D, Desai J, Steiger S, et al. Activated platelets induce MLKL-driven neutrophil necroptosis and release of neutrophil extracellular traps in venous thrombosis[J]. Cell Death Discov, 2018, 4:6.

备注/Memo

备注/Memo:
基金项目:国家自然科学基金(81873524); 国家重点研发计划项目(2016YFC1100900)
通信作者:徐志云,E-mail:zhiyunx@hotmail.com
更新日期/Last Update: 2021-12-01