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Scheme depicting GDF3-drived protection against endotoxin-induced inflammation, cardiac dysfunction and mortality. Exogenous GDF3 binds to ALK4/5/7 where activates Smad2/3 and inhibits NLRP3 inflammasome, consequently suppresses macrophage pro-inflammatory phenotype (M1), leading to reduced inflammation, cardiac dysfunction, and mortality in endotoxin-induced septic mice.
