自噬在脓毒症心肌功能障碍发病机制中的作用研究进展

被引:6
作者
周颖 [1 ,2 ,3 ]
杨国辉 [2 ]
机构
[1] 贵州医科大学研究生院
[2] 贵州医科大学附属医院内科ICU
[3] 贵州省黔西南布依族苗族自治州人民医院呼吸科
关键词
脓毒症; 心肌功能障碍; 发病机制; 自噬; 干预作用;
D O I
暂无
中图分类号
R459.7 [急症、急救处理]; R542.2 [心肌疾病];
学科分类号
100201 [内科学]; 100231 [临床病理学];
摘要
脓毒症是重症监护病房的常见病,也是危重症患者的主要死因。脓毒症心肌功能障碍是脓毒症引起的心功能不全,是脓毒症的常见并发症。文章从炎性反应、心肌抑制因子、心肌细胞线粒体功能、氧化应激、钙离子泵、内质网应激、心肌细胞凋亡、心脏微血管功能、交感神经与β肾上腺素受体、补体等方面阐述脓毒症心肌功能障碍的发病机制,探讨自噬作用在以上各个发病机制中的干预作用。从自噬角度干预脓毒症心肌功能障碍的病理生理过程可能成为治疗该病的新靶点。
引用
收藏
页码:776 / 781
页数:6
相关论文
共 47 条
[31]
Apigenin Alleviates Endotoxin-Induced Myocardial Toxicity by Modulating Inflammation; Oxidative Stress; and Autophagy.[J] Li Fang;Lang Fangfang;Zhang Huilin;Xu Liangdong;Wang Yidan;Zhai Chunxiao;Hao Enkui Oxidative medicine and cellular longevity 2017,
[32]
Autophagy Primes Neutrophils for Neutrophil Extracellular Trap Formation during Sepsis.[J] Park So Young;Shrestha Sanjeeb;Youn Young-Jin;Kim Jun-Kyu;Kim Shin-Yeong;Kim Hyun Jung;Park So-Hee;Ahn Won-Gyun;Kim Shin;Lee Myung Goo;Jung Ki-Suck;Park Yong Bum;Mo Eun-Kyung;Ko Yousang;Lee Suh-Young;Koh Younsuck;Park Myung Jae;Song Dong-Keun;Hong Chang-Won American journal of respiratory and critical care medicine 2017,
[33]
Lipocalin-2 (NGAL) Attenuates Autophagy to Exacerbate Cardiac Apoptosis Induced by Myocardial Ischemia.[J] Sung Hye Kyoung;Chan Yee Kwan;Han Meng;Jahng James Won Suk;Song Erfei;Danielson Eric;Berger Thorsten;Mak Tak W;Sweeney Gary Journal of cellular physiology 2017,
[34]
Innate Immunity to Intracellular Pathogens: Balancing Microbial Elimination and Inflammation[J] Gabriel Mitchell;Ralph R. Isberg Cell Host & Microbe 2017,
[35]
Role of Endoplasmic Reticulum Stress; Autophagy; and Inflammation in Cardiovascular Disease[J] Cheng Zhang;Taha Wasim Syed;Renjing Liu;Renjing Liu;Jun Yu Frontiers in Cardiovascular Medicine 2017,
[36]
The synthetic antimicrobial peptide 19-2.5 attenuates septic cardiomyopathy and prevents down-regulation of SERCA2 in polymicrobial sepsis.[J] Martin Lukas;Horst Klemens;Chiazza Fausto;Oggero Silvia;Collino Massimo;Brandenburg Klaus;Hildebrand Frank;Marx Gernot;Thiemermann Christoph;Schuerholz Tobias Scientific reports 2016,
[37]
The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)[J] Mervyn Singer;Clifford S. Deutschman;Christopher Warren Seymour;Manu Shankar-Hari;Djillali Annane;Michael Bauer;Rinaldo Bellomo;Gordon R. Bernard;Jean-Daniel Chiche;Craig M. Coopersmith;Richard S. Hotchkiss;Mitchell M. Levy;John C. Marshall;Greg S. Martin;Steven M. Opal;Gordon D. Rubenfeld;Tom van der Poll;Jean-Louis Vincent;Derek C. Angus JAMA 2016,
[38]
Mitochondrial ROS Induces Cardiac Inflammation via a Pathway through mtDNA Damage in a Pneumonia-Related Sepsis Model.[J] Yao Xiao;Carlson Deborah;Sun Yuxiao;Ma Lisha;Wolf Steven E;Minei Joseph P;Zang Qun S PloS one 2015,
[39]
Role of extracellular histones in the cardiomyopathy of sepsis.[J] Kalbitz Miriam;Grailer Jamison J;Fattahi Fatemeh;Jajou Lawrence;Herron Todd J;Campbell Katherine F;Zetoune Firas S;Bosmann Markus;Sarma J Vidya;Huber-Lang Markus;Gebhard Florian;Loaiza Randall;Valdivia Hector H;Jalife José;Russell Mark W;Ward Peter A FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2015,
[40]
Autophagy-dependent PELI3 degradation inhibits proinflammatory IL1B expression.[J] Giegerich Annika Klara;Kuchler Laura;Sha Lisa Katharina;Knape Tilo;Heide Heinrich;Wittig Ilka;Behrends Christian;Brüne Bernhard;von Knethen Andreas Autophagy 2014,