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Published on: May 3, 2016
Targeting STAT3 signaling in kidney disease
Jesse Pace1, Praharshasai Paladugu1, Bhaskar Das2
1Division of Nephrology, Department of Medicine, Stony Brook University , Stony Brook, New York.
STAT3, a key protein in the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway, plays a detrimental role in kidney disease progression. Inhibiting STAT3 shows promise for treating kidney diseases, with ongoing research into pharmacological approaches.
Area of Science:
- Molecular Biology
- Cellular Signaling
- Nephrology
Background:
- The Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway regulates cellular responses.
- Signal transducer and activator of transcription 3 (STAT3) is implicated in cancers and autoimmune disorders.
- STAT3's role in kidney disease progression is a recent focus, despite known benefits of its inhibition in models.
Purpose of the Study:
- To review the detrimental role of dysregulated STAT3 activation in kidney diseases.
- To summarize the progress in treating kidney diseases via pharmacological STAT3 inhibition.
Main Methods:
- Review of existing literature on STAT3 signaling in kidney disease.
- Analysis of genetic studies demonstrating benefits of STAT3 inhibition.
- Examination of pharmacological STAT3 inhibitors developed for cancer and tested in kidney disease models.
Main Results:
- Dysregulated STAT3 activation contributes to various kidney diseases.
- Genetic studies confirm beneficial effects of STAT3 inhibition in kidney disease models.
- Limited but growing number of STAT3 inhibitors have been evaluated in kidney disease.
Conclusions:
- STAT3 is a key mediator in the pathogenesis of kidney diseases.
- Pharmacological inhibition of STAT3 represents a potential therapeutic strategy for kidney disease.
- Further research and clinical translation of STAT3 inhibitors are warranted for kidney disease treatment.
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