[1]胡梦弦 何贵新 王明远 秦伟彬 冯雨菲 郑国坤 黄振乐 文 琦.Hippo激酶级联调控心肌缺血再灌注损伤炎症细胞表型[J].大众科技,2020,22(11):67-69.
 Hippo Kinase Cascade Regulates Inflammatory Cell Phenotype in Myocardial Ischemia-Reperfusion Injury[J].Popular Science & Technology,2020,22(11):67-69.
点击复制

Hippo激酶级联调控心肌缺血再灌注损伤炎症 细胞表型()
分享到:

《大众科技》[ISSN:1008-1151/CN:45-1235/N]

卷:
22
期数:
2020年11
页码:
67-69
栏目:
医药与卫生
出版日期:
2020-11-20

文章信息/Info

Title:
Hippo Kinase Cascade Regulates Inflammatory Cell Phenotype in Myocardial Ischemia-Reperfusion Injury
作者:
胡梦弦1 何贵新2 王明远2 秦伟彬2 冯雨菲1 郑国坤1 黄振乐1 文 琦1
(1.广西中医药大学,广西 南宁 530299; 2.广西中医药大学第一附属医院,广西 南宁 530023)
关键词:
hippo激酶心肌再灌注损伤炎症反应T淋巴细胞巨噬细胞
Keywords:
hippo kinase myocardial reperfusion injury inflammatory response T lymphocytes macrophages
文献标志码:
A
摘要:
血管再通是目前治疗冠状动脉狭窄或梗塞的关键措施,积极有效的防治缺血再灌注损伤对患者的预后具有及其重要的意义。免疫炎性损伤被认为是心肌缺血损伤的重要危害因子,如何减轻炎症反应在这损伤中起着关键的作用。Hippo激酶级联能够通过各种信号通路并结合多个下游靶点对炎症细胞的增殖、分化及表型进行调控,从而降低炎症程度,达到抑制细胞的损伤。文章对Hippo激酶级联在调控炎症反应中的作用进行综述。
Abstract:
Vascular recanalization is a key measure in the treatment of coronary artery stenosis or infarction. It is of great significance for the prognosis of patients to actively and effectively prevent ischemia reperfusion injury. Immune inflammatory injury is considered as an important risk factor for myocardial ischemic injury. How to reduce inflammatory response plays a key role in this injury. Hippo kinase cascade regulates the proliferation, differentiation, and phenotype of inflammatory cells through a variety of signaling pathways combined with multiple downstream targets, thereby reducing inflammation and inhibiting cell damage. This paper reviews the role of Hippo kinase cascade in the regulation of inflammatory response.

参考文献/References:

[1] Wang Y, Dembowsky K, Chevalier E, et al. C-X-C motif chemokine receptor 4 blockade promotes tissue repair after myocardial infarction by enhancing regulatory T cell mobilization and immune-regulatory function[J]. Circulation, 2019, 139(15): 1798-1812. [2] Zhao B, Tumaneng K, Guan K L. The Hippo pathway in organ size control, tissue regeneration and stem cell self-renewal[J]. Nature Cell Biology, 2011, 13(8): 877-883. [3] Ke D, Fang J, Fan L, et al. Targeted deletion of regulatory T cells attenuates the protective effects of myocardial ischemic preconditioning in rats[J]. Scandinavian Cardiovascular Journal, 2015, 49(1): 64-71. [4] Parhar K, Millar V, Zochios V, et al. Clinical outcomes of patients undergoing primary percutaneous coronary intervention for acute myocardial infarction requiring the intensive care unit[J]. Journal of Intensive Care, 2018, 6: 5. [5] Ke D, Fang J, Fan L,et al. Regulatory T cells contribute to rosuvastatin-induced cardioprotection against ischemia- reperfusion injury[J]. Coronary Artery Disease 2013, 24(4): 334-341. [6] Xia N, Jiao J, Tang T T, et al. Activated regulatory T-cells attenuate myocardial ischaemia/reperfusion injury through a CD39-dependent mechanism[J]. Clinical Science, 2015, 128(10): 679-693 . [7] Zhao B, Li L, Lei Q, et al. The Hippo-YAP pathway in organ size control and tumorigenesis: an updated version[J]. Genes and Development, 2010, 24(9): 862-874. [8] Li C, Bi Y, Li Y, et al. Dendritic cell MST1 inhibits Th17 differentiation[J]. Nature Communications, 2017, 8: 14275. [9] Zhou Q, Li L, Zhao B, et al. The hippo pathway in heart development, regeneration, and diseases[J]. Circulation Research, 2015, 116(8): 1431-1447. [10] Kanai F, Marignani P A, Sarbassova D. TAZ: a novel transcriptional co-activator regulated by interactions with 14-3-3 and PDZ domain proteins[J]. The EMBO Journal, 2000, 19: 6778-6791. [11] Geng J, Yu S, Zhao H, et al. Publisher correction: The transcriptional coactivator TAZ regulates reciprocal differentiation of TH17 cells and Treg cells[J]. Nature Immunology, 2018, 19(9): 1036. [12] Huang X, Li Y, Fu M, et al. Polarizing macrophages in vitro[J]. Macrophages, 2018, 1784: 119-126. [13] 徐志鹏,左国平,靳建亮. 巨噬细胞异质性及其在炎症调控中的研究进展[J]. 细胞与分子免疫学杂志,2015,31(12): 1711-1714. [14] Hume D A. The many alternative faces of macrophage activation[J]. Frontiers in Immunology, 2015, 6: 370. [15] Swirski F K. Inflammation and repair in the ischaemic myocardium[J]. Hamostaseologie. 2015, 35(1): 34-36. [16] Heidt T, Courties G, Dutta P, et al. Diferential contribution of monocytes to heart macrophages in steady -state and after myocardial infarction[J]. Circulation Research, 2014, 115: 284-295. [17] Shiraishi M, Shintani Y, Shintani Y, et al. Alternatively activated macrophages determine repair of the infarcted adult murine heart[J]. Journal of Clinical Investigation, 2016, 126: 2151-2166. [18] Jia C, Chen H, Wei M, et al. Gold nanoparticle-based miR155 antagonist macrophage delivery restores the cardiac function in ovariectomized diabetic mouse model[J]. International Journal of Nanomedicine, 2017, 12: 4963-4979. [19] Wang L, Luo J Y, Li B, et al. Integrin-YAP/TAZ-JNK cascade mediates atheroprotective effect of unidirectional shear flow[J]. Nature, 2016, 540(7634): 579-582. [20] Liu M, Yan M, Li H, et al. Macrophage K63-linked ubiquitination of YAP promotes its nuclear localization and exacerbates atherosclerosis[J]. Cell Reports, 2020, 32(5): 107990. [21] Feng Y, Liang Y, Zh X, et al. The signaling protein Wnt5a promotes TGFβ1-mediated macrophage polarization and kidney fibrosis by inducing the transcriptional regulators Yap/Taz[J]. Journal of Biological Chemistr, 2018, 293(50): 19290-19302. [22] Xin Z, Li W, Wang S, et al. YAP aggravates inflammatory bowel disease by regulating M1/M2 macrophage polarization and gut microbial homeostasis[J]. Cell Reports, 2019, 27(4):1176-1189. [23] Ramos A, Camargo F D. The Hippo signaling pathway and stem cell biology[J]. Trends in Cell Biology, 2012, 22(7): 339, 46.

备注/Memo

备注/Memo:
【收稿日期】2020-09-09 【基金项目】国家自然科学基金地区基金项目(81960861);国家自然科学基金地区基金项目(81460712);广西科学重点研发计划项目课题(桂科AB19110006)。 【作者简介】胡梦弦(1995-),男,广西中医药大学在读硕士研究生,医师,研究方向为中西医结合心血管防治。 【通信作者】何贵新(1973-),男,广西中医药大学第一附属医院主任医师,博士研究生,研究方向为心血管疾病的防治。
更新日期/Last Update: 2020-12-17