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Updated: Jun 21, 2026
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Published on: August 17, 2022
Autoimmune myocarditis: past, present and future
Florian Leuschner1, Hugo A Katus, Ziya Kaya
1Department of Cardiology, University of Heidelberg, 69120 Heidelberg, Germany.
Insights
Inflammation and autoimmune responses drive heart failure progression. Understanding these mechanisms, particularly in myocarditis, is crucial for developing new diagnostic and therapeutic strategies targeting chemokines, cytokines, and T cell responses.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Pathophysiology
Background:
- Heart failure is a growing global health concern with significant morbidity and mortality.
- While some causes of heart failure are known, the molecular pathways driving its progression and ventricular remodeling remain unclear.
- Inflammation and autoimmune processes are implicated in various cardiovascular diseases, suggesting a role in heart failure pathogenesis.
Purpose of the Study:
- To review the role of inflammatory mechanisms in the progression of heart failure.
- To discuss the challenges in diagnosing and treating myocarditis, a condition linked to heart failure.
- To explore potential therapeutic targets for heart failure based on recent animal model findings.
Main Methods:
- Review of existing literature on myocarditis, dilated cardiomyopathy, and heart failure.
- Analysis of findings from current animal models of heart failure.
- Examination of experimental approaches for improving diagnosis and identifying drug targets.
Main Results:
- Myocardial infiltration by lymphocytes and mononuclear cells, elevated pro-inflammatory cytokines/chemokines, and autoantibodies are common in myocarditis and dilated cardiomyopathy.
- Animal models provide insights into the molecular mechanisms of heart failure progression.
- Specific targets including chemokines, cytokines, T cell responses, tolerance induction, and autoantibody development are highlighted.
Conclusions:
- Inflammatory and autoimmune responses are key contributors to progressive heart failure.
- Improved diagnostic and therapeutic strategies for heart failure are needed, particularly for myocarditis.
- Further research into molecular targets identified in animal models holds promise for future treatments.
Abstract:
Heart failure has become an increasingly prevalent disorder with considerable morbidity and mortality. While many causal mechanisms such as inherited cardiomyopathies, ischemic cardiomyopathy or muscular overload are easily identified in clinical practice, the molecular mechanisms that determine the progression of heart failure or ventricular remodelling are largely unknown. Autoimmune responses and inflammation are involved in the pathogenesis of many cardiovascular diseases. There is compelling evidence that inflammatory mechanisms may contribute to progressive heart failure. Thus, myocardial infiltration of lymphocytes and mononuclear cells, increased expression of pro-inflammatory chemokines and cytokines and circulating autoantibodies are frequently observed in myocarditis and dilated cardiomyopathy. In this review we give an overview on myocarditis and describe why diagnosis and treatment of myocarditis in the clinic can be difficult. We present current animal models and describe possible experimental approaches to improve diagnosis. Finally, we give an outlook on possible drug targets by describing the latest findings in the animal models focussing on chemokines and cytokines, T cell responses and interactions, tolerance induction and the development of autoantibodies.
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