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Lysophosphatidic Acid-Mediated Inflammation at the Heart of Heart Failure

  • Cardiac Biomarkers (AA Quyyumi, Section Editor)
  • Published:
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Abstract

Purpose of Review

The primary aim of this review is to provide an in-depth examination of the role bioactive lipids—namely lysophosphatidic acid (LPA) and ceramides—play in inflammation-mediated cardiac remodeling during heart failure. With the global prevalence of heart failure on the rise, it is critical to understand the underlying molecular mechanisms contributing to its pathogenesis. Traditional studies have emphasized factors such as oxidative stress and neurohormonal activation, but emerging research has shed light on bioactive lipids as central mediators in heart failure pathology. By elucidating these intricacies, this review aims to:

  • Bridge the gap between basic research and clinical practice by highlighting clinically relevant pathways contributing to the pathogenesis and prognosis of heart failure.

  • Provide a foundation for the development of targeted therapies that could mitigate the effects of LPA and ceramides on heart failure.

  • Serve as a comprehensive resource for clinicians and researchers interested in the molecular biology of heart failure, aiding in better diagnostic and therapeutic decisions.

Recent Findings

Recent findings have shed light on the central role of bioactive lipids, specifically lysophosphatidic acid (LPA) and ceramides, in heart failure pathology. Traditional studies have emphasized factors such as hypoxia-mediated cardiomyocyte loss and neurohormonal activation in the development of heart failure. Emerging research has elucidated the intricacies of bioactive lipid-mediated inflammation in cardiac remodeling and the development of heart failure. Studies have shown that LPA and ceramides contribute to the pathogenesis of heart failure by promoting inflammation, fibrosis, and apoptosis in cardiac cells. Additionally, recent studies have identified potential targeted therapies that could mitigate the effects of bioactive lipids on heart failure, including LPA receptor antagonists and ceramide synthase inhibitors. These recent findings provide a promising avenue for the development of targeted therapies that could improve the diagnosis and treatment of heart failure.

Summary

In this review, we highlight the pivotal role of inflammation induced by bioactive lipid signaling and its influence on the pathogenesis of heart failure. By critically assessing the existing literature, we provide a comprehensive resource for clinicians and researchers interested in the molecular mechanisms of heart failure. Our review aims to bridge the gap between basic research and clinical practice by providing actionable insights and a foundation for the development of targeted therapies that could mitigate the effects of bioactive lipids on heart failure. We hope that this review will aid in better diagnostic and therapeutic decisions, further advancing our collective understanding and management of heart failure.

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Data Availability

No datasets were generated or analyzed during the current study.

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Funding

Dr. Abdel-Latif is supported by NIH Grant R01 HL124266.

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Authors and Affiliations

  1. Division of Cardiology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, 48105, USA

    Rajesh Chaudhary, Tahra Suhan & Ahmed Abdel-Latif

  2. Ann Arbor VA Healthcare System, 2215 Fuller Rd, Ann Arbor, MI, 48105, USA

    Rajesh Chaudhary, Tahra Suhan & Ahmed Abdel-Latif

  3. Department of Kinesiology, University of Saskatchewan, Saskatchewan, Canada

    Mahmud W. Tarhuni

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  1. Rajesh Chaudhary
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R.C., A.A-L., and T.S. wrote the main manuscript text and R.C. prepared figure 1. M.W.T. reviewed and edited the manuscript. A.A-L. reviewed and edited the manuscript. All authors reviewed the manuscript.

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Correspondence to Ahmed Abdel-Latif.

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Chaudhary, R., Suhan, T., Tarhuni, M.W. et al. Lysophosphatidic Acid-Mediated Inflammation at the Heart of Heart Failure. Curr Cardiol Rep 26, 113–120 (2024). https://doi.org/10.1007/s11886-024-02023-8

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