ArticleJCI insight2022
Cardiac macrophages regulate isoproterenol-induced Takotsubo-like cardiomyopathy.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Role of Macrophages in Cardiac Remodeling: Cues From Zebrafish Heart.Immunity, inflammation and disease · 2026Pooled it
- P2X7-NEK7-NLRP3 Axis Drives Cardiac Inflammation and Fibrosis in Isoproterenol-Induced Cardiac Remodeling in Mice.Acta physiologica (Oxford, England) · 2026Article
- Review
- Coronary Microvascular Dysfunction in Stress Cardiomyopathy: At the Heart of the Problem.Life (Basel, Switzerland) · 2026Review
- Takotsubo syndrome: pathophysiological insights and innovations in patient care.Nature reviews. Cardiology · 2026Review
- The role of cellular senescence-related genes in ischemia-reperfusion injury and the identification of their biomarkers.Scientific reports · 2026Article
- Adrenergic receptors on immune cells in cardiovascular disease: signaling plasticity, biased agonism, and therapeutic opportunities.Frontiers in physiology · 2026Review
- Takotsubo syndrome as initial presentation of pheochromocytoma in young children: case report and literature review.BMC pediatrics · 2025Review
- The Genetic Puzzle of the Stress-Induced Cardiomyopathy (Takotsubo Syndrome): State of Art and Future Perspectives.Biomolecules · 2025Review
- Mortality risk stratification for Takotsubo syndrome: Evaluating CRP measurement alongside the InterTAK prognostic score.ESC heart failure · 2025Article
- The cellular and molecular cardiac tissue responses in human inflammatory cardiomyopathies after SARS-CoV-2 infection and COVID-19 vaccination.Nature cardiovascular research · 2025Article
- Myocarditis Mimicking Takotsubo Cardiomyopathy With First Dose of Neoadjuvant Nivolumab-Relatlimab.Case reports in oncological medicine · 2025Article
- Article
- Review
- In a Canine Model of Septic Shock, Cardiomyopathy Occurs Independent of Catecholamine Surges and Cardiac Microvascular Ischemia.Journal of the American Heart Association · 2024Article
- The role of inflammation in takotsubo syndrome: A new therapeutic target?Journal of cellular and molecular medicine · 2024Review
- Insulin resistance in Takotsubo syndrome.ESC heart failure · 2024Article
- Liraglutide Protects Cardiomyocytes against Isoprenaline-Induced Apoptosis in Experimental Takotsubo Syndrome.Biomedicines · 2024Article
- Monocyte-Derived Macrophages Aggravate Cardiac Dysfunction After Ischemic Stroke in Mice.Journal of the American Heart Association · 2024Article
- Treatment with β-Adrenoceptor Agonist Isoproterenol Reduces Non-parenchymal Cell Responses in LPS/D-GalN-Induced Liver Injury.Inflammation · 2024Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 3 countries.
Funding
Abstract
Takotsubo syndrome (TTS) is an acute, stress-induced cardiomyopathy that occurs predominantly in women after extreme physical and/or emotional stress. To date, our understanding of the molecular basis for TTS remains unknown and, consequently, specific therapies are lacking. Myocardial infiltration of monocytes and macrophages in TTS has been documented in clinical studies. However, the functional importance of these findings remains poorly understood. Here, we show that a single high dose of isoproterenol (ISO) in mice induced a TTS-like cardiomyopathy phenotype characterized by female predominance, severe cardiac dysfunction, and robust myocardial infiltration of macrophages. Single-cell RNA-Seq studies of myocardial immune cells revealed that TTS-like cardiomyopathy is associated with complex activation of innate and adaptive immune cells in the heart, and macrophages were identified as the dominant immune cells. Global macrophage depletion (via clodronate liposome administration) or blockade of macrophage infiltration (via a CCR2 antagonist or in CCR2-KO mice) resulted in recovery of cardiac dysfunction in ISO-challenged mice. In addition, damping myeloid cell activation by HIF1α deficiency or exposure to the immunomodulatory agent bortezomib ameliorated ISO-induced cardiac dysfunction. Collectively, our findings identify macrophages as a critical regulator of TTS pathogenesis that can be targeted for therapeutic gain.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.