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Published on: February 17, 2018
The Cardiohepatic Axis in Heart Failure
Arick C Park1, Joel D Schilling2
1Department of Internal Medicine, Washington University School of Medicine in St Louis, St. Louis, Missouri, USA.
Insights
Cardiogenic liver disease, a consequence of heart failure, causes liver dysfunction. Further research is needed to understand the underlying mechanisms of liver fibrosis and dysfunction in heart failure patients.
Area of Science:
- Cardiology
- Hepatology
- Pathology
Background:
- Cardiogenic liver disease results from hepatic congestion due to right heart failure.
- It leads to hepatic dysfunction and liver remodeling.
- Understanding liver pathology in heart failure is crucial for patient care.
Purpose of the Study:
- To review current understanding of the cardiohepatic axis in heart failure.
- To highlight knowledge gaps in cardiogenic liver disease.
- To identify opportunities for future research.
Main Methods:
- Review of recent human and preclinical data.
- Analysis of cellular and molecular pathways involved in cardiogenic liver disease.
Main Results:
- Liver congestion triggers significant responses in hepatocytes and nonparenchymal cells.
- Pathways driving liver fibrosis and dysfunction remain poorly understood.
- Emerging data is beginning to elucidate the cellular and molecular landscape.
Conclusions:
- Cardiogenic liver disease is a complex condition requiring further investigation.
- Elucidating the mechanisms of liver fibrosis and dysfunction is essential.
- Future research should focus on the cardiohepatic axis to improve patient outcomes.
Abstract:
Cardiogenic liver disease is a sequela of hepatic congestion from right heart failure that leads to hepatic dysfunction and adverse liver remodeling. Understanding the mechanisms and consequences of liver pathology in the syndrome of heart failure is an important unmet need in the care of patients with chronic heart failure. Liver congestion provokes profound responses in hepatocytes and nonparenchymal cells including endothelial cells, macrophages, and hepatic stellate cells. However, the pathways that drive liver fibrosis and dysfunction are poorly understood. Recent human and preclinical data has begun to unravel the cellular landscape and molecular pathways that define cardiogenic liver disease. This review aims to discuss our current understanding of the cardiohepatic axis in heart failure while also highlighting knowledge gaps and opportunities for future investigation.
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