Annexin A1 and specialized proresolving lipid mediators: promoting resolution as a therapeutic strategy in human inflammatory diseases

被引:35
|
作者
Perucci, Luiza Oliveira [1 ,2 ]
Sugimoto, Michelle Amantea [1 ,3 ]
Gomes, Karina Braga [1 ,2 ]
Dusse, Luci Maria [1 ,2 ,3 ]
Teixeira, Mauro Martins [4 ]
Sousa, Lirlandia Pires [1 ,2 ,3 ]
机构
[1] Univ Fed Minas Gerais, Fac Farm, Dept Anal Clin & Toxicol, Belo Horizonte, MG, Brazil
[2] Univ Fed Minas Gerais, Programa Posgrad Anal Clin & Toxicol, Belo Horizonte, MG, Brazil
[3] Univ Fed Minas Gerais, Programa Posgrad Ciencias Farmaceut, Belo Horizonte, MG, Brazil
[4] Univ Fed Minas Gerais, Inst Ciencias Biol, Dept Bioquim & Imunol, Belo Horizonte, MG, Brazil
关键词
Annexin A1; human inflammatory diseases; resolution of inflammation; specialized proresolving lipid mediators; MYOCARDIAL-ISCHEMIA-REPERFUSION; VISCERAL ADIPOSE-TISSUE; EXPERIMENTALLY-INDUCED COLITIS; POLYUNSATURATED FATTY-ACIDS; CORONARY-ARTERY-DISEASE; FORMYL PEPTIDE RECEPTOR; 2/LIPOXIN A(4) RECEPTOR; SULFATE-INDUCED COLITIS; CYSTIC-FIBROSIS AIRWAY; TRIGGERED RESOLVIN D1;
D O I
10.1080/14728222.2017.1364363
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Introduction: The timely resolution of inflammation is essential to restore tissue homeostasis and to avoid chronic inflammatory diseases. Resolution of inflammation is an active process modulated by various proresolving mediators, including annexin A1 (AnxA1) and specialized proresolving lipid mediators (SPMs), which counteract excessive inflammatory responses and stimulate proresolving mechanisms. Areas covered: The protective effects of AnxA1 and SPMs have been extensively explored in pre-clinical animal models. However, studies investigating the function of these molecules in human diseases are just emerging. This review highlights recent advances on the role of proresolving mediators, and pharmacological opportunities of promoting resolution pathways in preclinical models and patients with various human diseases. Expert opinion: Dysregulation or 'failure' in proresolving mechanisms might be involved in the pathogenesis of chronic inflammatory diseases. Altered levels of proresolving mediators were found in a wide range of human diseases. In some cases, AnxA1 and SPMs are up-regulated in human blood and tissues but fail to engage in proresolving signaling and, hence, to regulate excessive inflammation. Thus, the new concept of 'resolution pharmacology' could be applied to compensate deficiency of endogenous proresolving mediators' generation and/or possible failures in the engagement of resolution pathways observed in many chronic inflammatory diseases.
引用
收藏
页码:879 / 896
页数:18
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