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.

PubMed

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.

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