The suppressor of cytokine signaling–1 (SOCS1) is a novel therapeutic target for enterovirus-induced cardiac injury
J. Clin. Invest. Hideo Yasukawa, et al. 111:469 doi:10.1172/JCI16491 [Go to this article.]

Figure 7
JAK-STAT antiviral defense in the cardiac myocyte and SOCS inhibition to limit early virus-induced cardiac injury. (a) Virus infection of the heart stimulates cytokine-receptor signaling through the JAK-STAT pathway. Activation of the JAK-STAT pathway induces antiviral target gene transcription stimulating the innate viral defense in the cardiac myocyte. (b) While activation of the JAK-STAT pathway has an important role in antiviral defense, phosphorylated STAT also induces SOCS expression that attenuates the innate antiviral defense by inhibiting JAK signaling. As in SOCS1-transgenic mice, increased expression of SOCS in cardiac myocytes results in robust virus replication and cardiac injury. (c) The strategies aimed at inhibition of SOCS potentiate the innate antiviral actions of cytokines that utilize the JAK-STAT pathway, resulting in the prevention of virus-mediated myocardial injury. P, phosphorylated.