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. 2020 Sep 30;41(12):1525–1530. doi: 10.1038/s41401-020-00529-9

Fig. 1. Metrnl regulates the intracellular signaling pathway.

Fig. 1

In neurocytes, Metrnl protein promotes neurite outgrowth via the JAK-STAT3 and MEK-ERK signaling pathways. In adipocytes, overexpression of Metrnl enhances lipid metabolism, relieves high-fat diet-induced inflammation, and improves adipose remodeling through upregulation of PPARγ, subsequently improving insulin resistance. In myocytes, Metrnl protein upregulates PPARδ and promotes the phosphorylation of AMPK by increasing intracellular calcium and further promotes the phosphorylation of TBC1D1, HDAC5, and p38 MAPK in an AMPK-mediated manner, subsequently promoting expression and translocation of GLUT4, improving insulin sensitization and reducing inflammation. In naïve/M0-like bone marrow-derived macrophages, Metrnl protein increases STAT3 phosphorylation, promotes macrophage differentiation to an anti-inflammatory phenotype, and releases insulin-like growth factor 1, subsequently increasing primary muscle satellite cell proliferation and skeletal muscle repair.