Unified Nexus of Macrophages and Maresins in Cardiac Reparative Mechanisms
Document Type
Review
Publication Date
10-1-2018
Keywords
Inflammation, Myocardial infarction, Myocardium regeneration, Myocardium repair, Resolution of inflammation
Digital Object Identifier (DOI)
https://doi.org/10.1096/fj.201800254R
Abstract
Macrophages are immune-sensing "big eater" phagocytic cells responsible for an innate, adaptive, and regenerative response. Aftermyocardial infarction,macrophages predominantly clear the deceased cardiomyocyte apoptotic or necrotic neutrophils to develop a regenerative and reparative program with the activation of the lipoxygenase-mediated maresin (MaR) metabolome at the site of ischemic injury. The specialized proresolving molecule and macrophage mediator in resolving inflammation, MaR-1, produced by human macrophages, has potent defining effects that limit polymorphonuclear neutrophil infiltration, enhance uptake of apoptotic PMNs, regulate inflammation resolution and tissue regeneration, and reduce pain. In addition to proresolving and antiinflammatory actions, MaR-1 displays potent tissue regenerative effects in stroke and is an antinociceptive. Macrophages actively participate in the biosynthesis of bioactive MaR-2, which exhibits anti-inflammatory, proresolving, and atherosclerotic effects. A new class of macrophage-derived molecules, MaR conjugates in tissue regeneration, is identified that regulates phagocytosis and the repair and regeneration of damaged tissue. The presented reviewprovides a current summary of the effect ofMaRin resolution pathophysiology,with relevance to a cardiac repair program.
Was this content written or created while at USF?
No
Citation / Publisher Attribution
FASEB Journal, v. 32, issue 10, p. 5227-5237
Scholar Commons Citation
Jadapalli, Jeevan Kumar and Halade, Ganesh V., "Unified Nexus of Macrophages and Maresins in Cardiac Reparative Mechanisms" (2018). Internal Medicine Faculty Publications. 20.
https://digitalcommons.usf.edu/intmed_facpub/20
