Abstract
In this issue, Ying etal. show that p38α kinase (MAPK14) controls macrophage polarization following acute liver injury. Myeloid cell-specific depletion of p38α promotes polarization to anti-inflammatory M2 macrophages and prevents pro-inflammatory cytokine secretion that ameliorate acute liver injury and promotes hepatocyte proliferation. Therapeutic targeting of macrophage p38α is an attractive strategy not only to suppress inflammation, but also to support liver regeneration.
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