20 research outputs found
Characterizing the anti-inflammatory and tissue protective actions of a novel Annexin A1 peptide
This work was supported by a
collaborative project between Unigene Corp. and
Queen Mary University of London and by the
William Harvey Research Foundation. JD is
supported by a Sir Henry Dale Fellowship jointly
funded by the Wellcome Trust and the Royal
Society (grant no: 107613/Z/15/Z). MP was
supported by the Wellcome Trust (grant no:
086867/Z/08)
Neutralizing monoclonal antibodies recognize antigenic variants among isolates of infectious hematopoietic necrosis virus
Sequence analysis and identification of new isoform of EP4 receptors in different atlantic salmon tissues (salmo salar l.) and its role in PGE2 induced immunomodulation in vitro
A DNA fluorometric assay for measuring fish cell proliferation in microplates with different well sizes
Specialized Pro-Resolving Mediators Directs Cardiac Healing and Repair with Activation of Inflammation and Resolution Program in Heart Failure
After myocardial infarction, splenic leukocytes direct biosynthesis of specialized pro-resolving mediators (SPMs) that are essential for the resolution of inflammation and tissue repair. In a laboratory environment, after coronary ligation of healthy risk free rodents (young adult mice) leukocytes biosynthesize SPMs with induced activity of lipoxygenases and cyclooxygenases, which facilitate cardiac repair. Activated monocytes/macrophages drive the biosynthesis of SPMs following experimental myocardial infarction in mice during the acute heart failure. In the presented review, we provided the recent updates on SPMs (resolvins, lipoxins and maresins) in cardiac repair that may serve as novel therapeutics for future heart failure therapy/management. We incorporated the underlying causes of non-resolving inflammation following cardiac injury if superimposed with obesity, hypertension, diabetes, disrupted circadian rhythm, co-medication (painkillers or oncological therapeutics), and/or aging that may delay or impair the biosynthesis of SPMs, intensifying pathological remodeling in heart failure