Macrophage-neutrophil crosstalk via the Selplg-Sell-YAP axis drives NETosis and MASH-associated liver fibrosis
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The authors investigate the immune mechanisms underlying the transition from inflammation to fibrosis in metabolic dysfunction-associated steatohepatitis (MASH), specifically focusing on the crosstalk between macrophages and neutrophils. They identify the Selplg-Sell-YAP signaling axis as a key driver of neutrophil extracellular trap (NET) formation, which subsequently activates hepatic stellate cells and promotes fibrosis. The study suggests that targeting this axis could offer therapeutic potential for MASH-associated liver fibrosis.
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