ArticleJACC. Basic to translational science2023
Recurrent Myocardial Injury Leads to Disease Tolerance in a Murine Model of Stress-Induced Cardiomyopathy.
Article in JACC. Basic to translational science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Review
- Comparative analysis of isoproterenol- and lipopolysaccharide-mediated cytoprotective responses in the heart.American journal of physiology. Heart and circulatory physiology · 2025Article
- Toll-like receptor 4 induces trained innate immune tolerance in the heart in a model of stress-induced cardiomyopathy.Cardiovascular research · 2025Article
- Review
- Development of a small animal model replicating core characteristics of takotsubo syndrome in humans.European heart journal open · 2024Article
- Animal models of Takotsubo syndrome: bridging the gap to the human condition.Frontiers in cardiovascular medicine · 2024Review
- Editorial: Reviews in takotsubo syndrome.Frontiers in cardiovascular medicine · 2024Article
- Recurrent Adrenergic Stress Provokes Persistent Myocarditis in PD-1-Deficient Mice.JACC. Basic to translational science · 2023Article
- Macrophages Remember When Your Heart Was Broken.JACC. Basic to translational science · 2023Article
- The Immunology of Takotsubo Syndrome.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Whereas the innate immune response to an initial episode of cardiac injury has been studied extensively, the response of the immune system to recurrent cardiac tissue injury is not well understood. Specifically, it is not known whether the immune system adapts to the initial episode of cardiac injury and whether any adaptations that occur lead to immune cell hypo-responsiveness or, alternatively, immune cell hyper-responsiveness. Here, we studied the role of adrenergic-mediated stress using a simple model of reversible stress-induced cardiomyopathy, and show that isoproterenol-induced tissue injury and inflammation are sufficient to protect the heart from the myopathic effects of a subsequent exposure to isoproterenol. Remarkably, pharmacological depletion of macrophages partially attenuated the isoproterenol-induced cytoprotective response, suggesting that immune-mediated tissue repair mechanisms confer tolerance to subsequent tissue damage.
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Registered trials
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