Biosynthesis of maresin-like SPMs

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R-HSA-9027307
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Homo sapiens
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Maresin-like mediators MaR-L1, Mar-L2 and 14,21-dihydroxy docosahexaenoic acids are normally synthesized by leukocytes, platelets and macrophages, via the pathways described here. Impaired production of these specialised proresolving mediators (SPMs) in diabetic skin wounds is associated with impaired macrophage function and delayed or absent wound healing (Brem & Tomic-Canic 2007, Boniakowski et al 2017). Macrophages play critical roles in wound healing by mechanisms as yet unknown. They are active in both the initiation (M1 macrophage phenotype) and the resolution (M2 macrophage phenotype) of inflammatory processes. In a pathological state, the switch from the M1 phenotype macrophage to the M2 phenotype macrophage may be delayed or fail to occur, which can result in chronic low-grade inflammation. This macrophage phenotype skewing toward an inflammatory phenotype has been implicated in the pathogenesis of type 2 diabetes (T2D) and the non-healing of diabetic wounds (Boniakowski et al 2017, Pradhan et al. 2009).

Administration of maresin-like SPMs to diabetic mice with induced wounds have been shown to act as autocrine/paracrine factors in restoring reparative functions of macrophages (Hong et al. 2014, Tian et al. 2011a, 2011b, Lu et al. 2010, Hellman et al. 2012).

Literature References
PubMed ID Title Journal Year
28630109 Macrophage-Mediated Inflammation in Normal and Diabetic Wound Healing

Boniakowski, AE, Kimball, AS, Jacobs, BN, Kunkel, SL, Gallagher, KA

J. Immunol. 2017
22374140 Proresolving lipid mediators and diabetic wound healing

Hellmann, J, Tang, Y, Spite, M

Curr Opin Endocrinol Diabetes Obes 2012
17476353 Cellular and molecular basis of wound healing in diabetes

Brem, H, Tomic-Canic, M

J. Clin. Invest. 2007
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