Mechanisms of cardiac ethanol toxicity and novel treatment options

Julian Mustroph1, Simon Lebek1, Lars S Maier1

  • 1Department of Internal Medicine II, University Medical Center Regensburg, Germany.

Pharmacology & Therapeutics
|December 18, 2018
PubMed

Insights

Ethanol harms the heart by disrupting cardiomyocyte function and predisposing to arrhythmias and heart failure. This review explores molecular mechanisms, focusing on reactive oxygen species (ROS) and druggable pathways for potential treatments.

Area of Science:

  • Cardiology
  • Toxicology
  • Molecular Biology

Background:

  • Ethanol consumption acutely and chronically impairs cardiac function.
  • Ethanol abuse is linked to arrhythmias and heart failure.
  • The molecular basis of ethanol's cardiac toxicity remains unclear.

Purpose of the Study:

  • To review current knowledge on molecular mechanisms of cardiac ethanol toxicity.
  • To focus on druggable pathways involved in ethanol's effects on the heart.
  • To provide a clinical outlook on potential novel treatment options.

Main Methods:

  • Review of existing literature on ethanol's cardiac effects.
  • Discussion of ethanol's impact on excitation-contraction coupling, oxidative stress, apoptosis, and metabolism.
  • Analysis of ethanol metabolites' role in cardiac toxicity.

Main Results:

  • Recent findings highlight the role of reactive oxygen species (ROS) in acute ethanol toxicity.
  • Ethanol induces sarcoplasmic reticulum (SR) Ca2+ leak via CaMKII-dependent pathways downstream of ROS.
  • Ethanol affects cardiac metabolism and promotes apoptosis.

Conclusions:

  • Understanding ethanol's molecular mechanisms is crucial for developing targeted therapies.
  • Druggable pathways, particularly those involving ROS and Ca2+ handling, offer therapeutic potential.
  • Further research into acute ethanol effects may reveal novel treatment strategies for alcoholic cardiomyopathy.

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