Key result
Maresin 1 (MaR1) mitigates nonalcoholic steatohepatitis (NASH) by reprograming macrophages to an antiinflammatory phenotype via the retinoic acid-related orphan receptor α (RORα).
The identification of the MaR1-RORα pathway as an endogenous protective mechanism against NASH may offer new therapeutic targets for metabolic diseases.
Chronic unresolved inflammation contributes to the development of nonalcoholic steatohepatitis (NASH), a disorder characterized by lipotoxicity, fibrosis, and progressive liver dysfunction. In this issue of the JCI, Han et al. report that maresin 1 (MaR1), a proresolving lipid mediator, mitigates NASH by reprograming macrophages to an antiinflammatory phenotype. Mechanistically, they identified retinoic acid-related orphan receptor α (RORα) as both a target and autocrine regulator of MaR1 production. Because NASH is associated with many widely occurring metabolic diseases, including obesity and type 2 diabetes, identification of this endogenous protective pathway could have broad therapeutic implications.
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Matthew R. Spite (2019) conducted an editorial in Nonalcoholic steatohepatitis (NASH). Maresin 1 (MaR1) was evaluated. Maresin 1 (MaR1) mitigates nonalcoholic steatohepatitis (NASH) by reprograming macrophages to an antiinflammatory phenotype via the retinoic acid-related orphan receptor α (RORα).
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