Molecular mechanism and therapeutic modulation of high mobility group box 1 release and action: an updated review

被引:160
作者
Lu, Ben [1 ,2 ,3 ]
Wang, Ce [4 ]
Wang, Mao [5 ]
Li, Wei [2 ,3 ]
Chen, Fangping [1 ]
Tracey, Kevin J. [2 ,3 ]
Wang, Haichao [2 ,3 ,6 ]
机构
[1] Cent South Univ, Xiangya Hosp 3, Dept Hematol, Changsha, Hunan, Peoples R China
[2] North Shore LIJ Hlth Syst, Feinstein Inst Med Res, Great Neck, NY 11030 USA
[3] North Shore LIJ Hlth Syst, Hofstra North Shore LIJ Sch Med, Great Neck, NY 11030 USA
[4] 4th Mil Med Univ, Sch Pharm, Xian, Shaanxi, Peoples R China
[5] St Johns Univ, Dept Pharmaceut Sci, Jamaica, NY 11439 USA
[6] N Shore Univ Hosp, Dept Emergency Med, Manhasset, NY 11030 USA
关键词
damage-associated molecular patterns; herbal components; high mobility group box 1; infection; injury; pathogen-associated molecular patterns; signaling; HMGB1-INDUCED INFLAMMATORY RESPONSES; ISCHEMIA-REPERFUSION INJURY; CHROMOSOMAL-PROTEIN; ACUTE LUNG INJURY; LETHAL SEPSIS; HMGB1; RELEASE; INHIBITS HMGB1; TNF-ALPHA; RAT MODEL; ISCHEMIA/REPERFUSION INJURY;
D O I
10.1586/1744666X.2014.909730
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
High mobility group box 1 (HMGB1) is an evolutionarily conserved protein, and is constitutively expressed in virtually all types of cells. Infection and injury converge on common inflammatory responses that are mediated by HMGB1 secreted from immunologically activated immune cells or passively released from pathologically damaged cells. Herein we review the emerging molecular mechanisms underlying the regulation of pathogen-associated molecular patterns (PAMPs)-induced HMGB1 secretion, and summarize many HMGB1-targeting therapeutic strategies for the treatment of infection- and injury-elicited inflammatory diseases. It may well be possible to develop strategies that specifically attenuate damage-associated molecular patterns (DAMPs)-mediated inflammatory responses without compromising the PAMPs-mediated innate immunity for the clinical management of infection- and injury-elicited inflammatory diseases.
引用
收藏
页码:713 / 727
页数:15
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