Resolving Inflammation in Heart Failure: Novel Protective Lipid Mediators

被引:10
|
作者
Reina-Couto, Marta [1 ,2 ,3 ]
Vale, Luis [1 ]
Carvalho, Jorge [1 ]
Bettencourt, Paulo [4 ,5 ]
Albino-Teixeira, Antonio [1 ,2 ]
Sousa, Teresa [1 ,2 ]
机构
[1] Univ Porto, Dept Farmacol & Terapeut, Fac Med, Rua Dr Placido da Costa 91,Piso 3, P-4200450 Oporto, Portugal
[2] Univ Porto, MedInUP Ctr Invest Farmacol & Inovacao Medicament, Alameda Prof Hernani Monteiro, P-4200319 Oporto, Portugal
[3] Ctr Hosp Sao Joao, Dept Med Intens, Alameda Prof Hernani Monteiro, P-4200319 Oporto, Portugal
[4] Ctr Hosp Sao Joao, Dept Med Interna, Alameda Prof Hernani Monteiro, P-4200319 Oporto, Portugal
[5] Univ Porto, Dept Med, Fac Med, Alameda Prof Hernani Monteiro, P-4200319 Oporto, Portugal
关键词
Heart failure; resolution of inflammation; proresolving lipid mediators; cardiovascular/metabolic and renal protection; therapeutic modulation; ASPIRIN-TRIGGERED LIPOXIN; 15-EPI-LIPOXIN A(4) PRODUCTION; REVERSE CHOLESTEROL TRANSPORT; IN-VIVO; ANTIINFLAMMATORY ACTIONS; MYOCARDIAL-INFARCTION; APOPTOTIC NEUTROPHILS; DOCOSAHEXAENOIC ACID; REPERFUSION INJURY; ENDOTHELIAL-CELLS;
D O I
10.2174/1389450117666160101121135
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Inflammation is an important pathogenic mechanism in chronic heart failure (HF). The perpetuation of the inflammatory response in this syndrome may result either from excessive activation of proinflammatory cascades or disturbances in the resolution of inflammation. However, although cardiovascular research has extensively investigated the proinflammatory processes involved in chronic HF pathophysiology, the mechanisms responsible for inflammation resolution in this disease remain largely disregarded. The resolving response is currently considered an active process involving specific effectors that limit the progression of inflammation and promote tissue regeneration. This article aims at reviewing the major classes of lipid mediators of inflammation resolution, their cardiovascular, metabolic and renal protective effects that might putatively delay the onset and progression of chronic HF, and their therapeutic modulation. Furthermore, it also aims to emphasize the importance of adopting therapeutic strategies that stimulate the resolution of inflammation in chronic HF.
引用
收藏
页码:1206 / 1223
页数:18
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