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Published on: December 2, 2016
STAT3 and cardiac remodeling
Arash Haghikia1, Britta Stapel, Melanie Hoch
1Department of Cardiology and Angiology, Medical School Hannover, Carl-Neuberg-Str. 1, 30625, Hannover, Germany.
Insights
The signal transducer and activator of transcription 3 (STAT3) protein influences heart remodeling and function. STAT3 signaling is a potential therapeutic target for cardiac conditions.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Cell Signaling
Background:
- The signal transducer and activator of transcription 3 (STAT3) protein plays a role in cardiomyocyte protection and hypertrophy.
- STAT3 signaling impacts cardiac remodeling through paracrine pathways affecting vasculature and extracellular matrix.
Purpose of the Study:
- To review the role of STAT3 signaling in cardiac remodeling.
- To summarize current understanding of STAT3's function in cardiac physiology and pathophysiology.
- To discuss STAT3 as a potential therapeutic target for cardiac remodeling.
Main Methods:
- Review of in vitro and in vivo studies.
- Analysis of experimental and clinical data on STAT3 in cardiac remodeling.
- Literature synthesis on STAT3's molecular and cellular mechanisms.
Main Results:
- STAT3 is involved in cardiomyocyte protection, hypertrophy, and cardiac remodeling.
- STAT3 is activated by various factors like cytokines, growth factors, and ischemia.
- STAT3 functions as a signaling molecule, transcription factor, and mitochondrial protein.
Conclusions:
- STAT3 signaling is crucial for cardiac remodeling in both physiological and pathological states.
- STAT3's multifaceted roles in the heart highlight its significance.
- Targeting STAT3 signaling presents a promising therapeutic strategy for cardiac remodeling.
Abstract:
Multiple in vitro and in vivo studies showed that the signal transducer and activator of transcription 3 (STAT3) protein is involved in cardiomyocyte protection and hypertrophy and via paracrine pathways impacts on the non-myocyte compartment, i.e., the vasculature and the extracellular matrix. In this regard, STAT3 interacts with a broad range of cellular and molecular mechanisms that direct remodeling processes in cardiac physiology (exercise, pregnancy) and pathophysiology (pressure overload, ischemia/reperfusion, myocardial infarction, and cardiotoxic agents). STAT3 is constitutively activated by a multitude of factors including cytokines, growth factors, neurohormones, mechanical load, and ischemia. It acts as a signaling molecule, a transcription factor and according to latest observations as a mitochondrial protein involved in energy production. In this review, we provide an overview on STAT3 signaling and summarize the current understanding of the role of STAT3 for different aspects of cardiac remodeling obtained from numerous experimental and clinical studies. Finally, we highlight and critically discuss STAT3 signaling as a possible target for future therapeutic approaches in the setting of cardiac remodeling.
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