Key result
Suppressor of cytokine signaling (SOCS) proteins negatively regulate Jak/STAT signaling and offer therapeutic potential to control heart failure progression and limit myocardial depression.
SOCS proteins are underexplored negative regulators of Jak/STAT signaling that may hold therapeutic potential for limiting myocardial depression and controlling heart failure progression.
SOCS modulation remains investigational in HF; leaves open clinical translation pending prospective trials.
Cytokines are important mediators of cardiac disease. Accumulating evidence indicates that members of the interleukin-6 family of cytokines promote cardiac hypertrophy through the activation of the Janus kinase-signal transducer and activator of transcription (Jak/STAT) pathway. Aberrant Jak/STAT signaling may promote progression from hypertrophy to heart failure. Suppressor of cytokine signaling (SOCS) proteins are underexplored, negative regulators of Jak/STAT signaling. SOCS proteins may also interact with other inflammatory pathways known to affect cardiac function. A better understanding of the therapeutic potential of these proteins may lead to the controlled progression of heart failure and the limitation of myocardial depression. This review summarizes the cardiophysiological effect of the IL-6 cytokine family, outlines the mechanistic pathway of Jak/STAT signaling, explores the regulatory role of SOCS proteins in the heart, and discusses the potential of using SOCS proteins clinically.
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Terrell et al. (2006) conducted a review in Cardiac disease. SOCS proteins was evaluated. Suppressor of cytokine signaling (SOCS) proteins negatively regulate Jak/STAT signaling and offer therapeutic potential to control heart failure progression and limit myocardial depression.
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