The Role Of Stats Activation In Kidney Proximal Tubule Epithelial Apoptosis Following Ischemia/reperfusion Injury And Its Intracellular Mechanisms

Background and objective Acute renal failure (ARF) remains a common clinical entity and results in unacceptable high mortality among hospitalized patients, especially in the intensive care unit setting. Despite advances in medical care, the outcome has not improved during the past 50 years. Acute renal failure(ATN) is the most common form of ARF and is characterized by tubular cell death. Recent evidence suggests that apoptosis is the primary mode of tubular cell death found in ATN and apoptosis is an important therapeutic target in ATN. Unfortunately, the molecular basis underlying apoptosis during ATN is largely unknown. It is important to understand the intracellular signaling pathways that are involved in apoptosis in ATN. Janus kinase-signal transducers and activators of transcription(Jak-Stat) pathway participates in imflammation, apoptosis, proliferation, tumorigenesis and negatively regulated by the family of suppressors of cytokine signaling ( SOCS ) . To our knowledge , there have been no reports regarding the role of Jak-Stat-SOCS in ATN and their contribution to tubular cell apoptosis. The present study was conducted to examine the role of the Jak-Stat-SOCS pathway in kidney proximal tubular epithelial cell apoptosis following ischemia and reperfusion injury (IRI) , and hopefully, to open a new therapeutic modality to mitigate the development of ATN.