JAK/STAT/SOCS signaling circuits and associated cytokine-mediated inflammation and hypertrophy in the heart

Andrew M. Terrell, Paul R. Crisostomo, George M. Wairiuko, Meijing Wang, Eric D. Morrell, Daniel R. Meldrum

Research output: Contribution to journalReview article

73 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)226-234
Number of pages9
JournalShock
Volume26
Issue number3
DOIs
StatePublished - Sep 1 2006

Keywords

  • IL-6
  • Janus kinase
  • Suppressor of cytokine signaling

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine
  • Physiology

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