JAK-STAT pathway in cardiac ischemic stress.
In our quest for comprehensive protection of ischemic myocardium, both basic and clinical studies have lead us to examine signal transduction pathways involved in ischemia-reperfusion injury for potential therapeutic targets. In this review, we have highlighted the importance of the JAK-STAT pathway in modulating ischemia-reperfusion injury. The mechanisms linking glucose metabolism, angiotensin II, with JAK-STAT pathway in ischemic injury are explored in this review. Clearly, the studies discussed in this review provide rationale for the design and synthesis of selective blockers of JAK-STAT pathway as potential therapeutic adjuncts in protecting ischemic myocardium.
Ananthakrishnan
Radha
R
Division of Surgical Science, Department of Surgery, College of Physicians and Surgeons 17-401, Columbia University, New York, NY 10032, USA.
Hallam
Kellie
K
Li
Qing
Q
Ramasamy
Ravichandran
R
D000818:Animals; D005947:Glucose / Q000502:physiology; D006333:Heart Failure / Q000503:physiopathology; D006801:Humans; D019157:Ischemic Preconditioning, Myocardial; D053616:Janus Kinase 3; D017202:Myocardial Ischemia / Q000503:physiopathology*; D011505:Protein-Tyrosine Kinases / Q000502:physiology*; D012084:Renin-Angiotensin System / Q000502:physiology; D050791:STAT Transcription Factors / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology*; D013312:Stress, Physiological / Q000503:physiopathology*
D050791:STAT Transcription Factors; D011505:Protein-Tyrosine Kinases; C507933:JAK3 protein, human; D053616:Janus Kinase 3; D005947:Glucose