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Published on: August 7, 2012
Hepatokines and their role in cardiohepatic interactions in heart failure
Wael A Shouman1, Sarah Najmeddine1, Lilas Sinno1
1Department of Pharmacology and Toxicology, American University of Beirut Faculty of Medicine, Beirut, Lebanon.
Insights
Hepatokines, proteins from the liver, are increasingly recognized for their role in heart failure. Understanding these factors is crucial for improving patient outcomes and developing new treatments.
Area of Science:
- Cardiovascular Medicine
- Hepatology
- Metabolic Regulation
Background:
- Heart failure is a global health crisis impacting multiple organ systems.
- The liver plays a significant role in heart failure pathogenesis, with conditions like cardiac hepatopathy and cirrhotic cardiomyopathy linked to poor prognosis.
- Existing knowledge gaps exist regarding the influence of hepatocyte-derived proteins and metabolic regulators on heart failure progression and associated complications.
Purpose of the Study:
- To identify key hepatokines (adropin, fetuin-A, fetuin-B, FGF-21, selenoprotein P, α1-microglobulin) implicated in heart failure.
- To explore the role of these hepatokines as modulators of metabolic homeostasis and cardiac dysfunction.
- To synthesize current research on hepatokine involvement in adverse cardiac remodeling, fibrosis, cachexia, and renal dysfunction.
Main Methods:
- Literature review of studies investigating hepatokines in heart failure.
- Analysis of proposed mechanisms by which hepatokines influence cellular processes.
- Identification of specific hepatokines under investigation for their role in cardiac dysfunction.
Main Results:
- Several hepatokines, including adropin, fetuin-A, fetuin-B, FGF-21, selenoprotein P, and α1-microglobulin, are being studied for their impact on heart failure.
- These factors are suggested to modulate critical pathways such as oxidative stress, fibrosis, apoptosis, inflammation, and mitochondrial function.
- Emerging evidence indicates their influence on immune responses, cellular migration, and overall metabolic homeostasis in the context of heart failure.
Conclusions:
- Hepatokines represent a significant area of research in understanding and potentially treating heart failure.
- Further investigation into the precise roles and clinical applications of these liver-derived factors is warranted.
- Targeting hepatokines may offer novel therapeutic strategies for managing heart failure and its complications.
Abstract:
Heart failure is one of the leading causes of death and disease worldwide. It is a condition that affects multiple systems within the body. There is a large body of evidence supporting that the liver is a major organ involved in the pathogenesis of heart failure. Cardiac hepatopathy and cirrhotic cardiomyopathy are two conditions that are associated with poor clinical outcomes in patients with heart failure. Despite the extensive proposed explanations of the mechanisms entailing heart failure, there remains a gap in the role of proteins and metabolic regulators produced by hepatocytes and their effect on the development, progression, and prognosis of heart failure, including adverse cardiac remodeling, fibrosis, cardiac cachexia, and renal dysfunction associated with heart failure. The aim of this review is to identify the major hepatokines being studied (adropin, fetuin-A, fetuin-B, FGF-21, selenoprotein P and α1-microglobulin) as modulators of metabolic homeostasis and cardiac dysfunction in heart failure. Research suggests that these factors play a role in modulating oxidative stress, fibrosis, apoptosis, inflammatory responses, immune cell activation, mitochondrial dysfunction, and cellular migration. The exact role of each of these hepatokines is under on-going research and requires more investigations for future clinical use.
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