ArticleCardiovascular research2022
Circulating microRNAs predispose to takotsubo syndrome following high-dose adrenaline exposure.
Article in Cardiovascular research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 3 of them syntheses 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.
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Who cites it
32 citing papers in PubMed, 3 syntheses or guidelines pooled it, 57 citations in OpenAlex.
- MicroRNAs in Takotsubo Syndrome: A Systematic Review of Regulatory Networks in Stress-Induced Cardiomyopathy.International journal of molecular sciences · 2025Pooled it
- Comparison of troponin and natriuretic peptides in Takotsubo syndrome and acute coronary syndrome: a meta-analysis.Open heart · 2024Pooled it
- Genetic and Epigenetic Factors of Takotsubo Syndrome: A Systematic Review.International journal of molecular sciences · 2021Pooled it
- Physical Exercise or Cognitive Behavioral Therapy for Takotsubo Cardiomyopathy: A Randomized Controlled Trial.Circulation. Heart failure · 2026Trial
- A Genome-Wide Association Study of Takotsubo Syndrome.JACC. Basic to translational science · 2026Article
- Takotsubo syndrome: pathophysiological insights and innovations in patient care.Nature reviews. Cardiology · 2026Review
- Oxidative Stress in Takotsubo Syndrome: Insights into Extracellular Vesicles and Their Potential Clinical Relevance.Antioxidants (Basel, Switzerland) · 2026Review
- Article
- Myocardial stunning: mechanisms, molecular insights, and gaps in knowledge.Bioscience reports · 2025Review
- The Role of MicroRNAs in the Pathophysiology and Management of Heart Failure: From Molecular Mechanisms to Clinical Application.International journal of molecular sciences · 2025Review
- miRNA-Orchestrated Fibroinflammatory Responses in Heart Failure with Preserved Ejection Fraction: Translational Opportunities for Precision Medicine.Diagnostics (Basel, Switzerland) · 2025Review
- The Genetic Puzzle of the Stress-Induced Cardiomyopathy (Takotsubo Syndrome): State of Art and Future Perspectives.Biomolecules · 2025Review
- "Restless Nights, Stressed Hearts": The Link Between Sleep Disorders and Takotsubo Syndrome-A Comprehensive Review.Reviews in cardiovascular medicine · 2025Review
- Exosomal mir-126-3p derived from endothelial cells induces ion channel dysfunction by targeting RGS3 signaling in cardiomyocytes: a novel mechanism in Takotsubo cardiomyopathy.Stem cell research & therapy · 2025Article
- The role of inflammation in takotsubo syndrome: A new therapeutic target?Journal of cellular and molecular medicine · 2024Review
- Exploratory Review of the Takotsubo Syndrome and the Possible Role of the Psychosocial Stress Response and Inflammaging.Biomolecules · 2024Review
- Heart-brain interactions: clinical evidence and mechanisms based on critical care medicine.Frontiers in cardiovascular medicine · 2024Review
- Animal models of Takotsubo syndrome: bridging the gap to the human condition.Frontiers in cardiovascular medicine · 2024Review
- Takotsubo syndrome: unravelling the enigma of the broken heart syndrome?-a narrative review.Cardiovascular diagnosis and therapy · 2023Review
- MicroRNAs: Midfielders of Cardiac Health, Disease and Treatment.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 3 countries.
Funding
Abstract
aimsTakotsubo syndrome (TTS) is an acute heart failure, typically triggered by high adrenaline during physical or emotional stress. It is distinguished from myocardial infarction (MI) by a characteristic pattern of ventricular basal hypercontractility with hypokinesis of apical segments, and in the absence of culprit coronary occlusion. We aimed to understand whether recently discovered circulating biomarkers miR-16 and miR-26a, which differentiate TTS from MI at presentation, were mechanistically involved in the pathophysiology of TTS. METHODS AND
resultsmiR-16 and miR-26a were co-overexpressed in rats with AAV and TTS induced with an adrenaline bolus. Untreated isolated rat cardiomyocytes were transfected with pre-/anti-miRs and functionally assessed. Ventricular basal hypercontraction and apical depression were accentuated in miR-transfected animals after induction of TTS. In vitro miR-16 and/or miR-26a overexpression in isolated apical (but not basal), cardiomyocytes produced strong depression of contraction, with loss of adrenaline sensitivity. They also enhanced the initial positive inotropic effect of adrenaline in basal cells. Decreased contractility after TTS-miRs was reproduced in non-failing human apical cardiomyocytes. Bioinformatic profiling of miR targets, followed by expression assays and functional experiments, identified reductions of CACNB1 (L-type calcium channel Cavβ subunit), RGS4 (regulator of G-protein signalling 4), and G-protein subunit Gβ (GNB1) as underlying these effects.
conclusionmiR-16 and miR-26a sensitize the heart to TTS-like changes produced by adrenaline. Since these miRs have been associated with anxiety and depression, they could provide a mechanism whereby priming of the heart by previous stress causes an increased likelihood of TTS in the future.
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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.