ReviewInternational journal of molecular medicine2025
Takotsubo syndrome: Unraveling the mystery behind its triggers (Review).
Review in International journal of molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Spontaneous Coronary Artery Dissection and Takotsubo Syndrome: Converging Mechanisms, Diagnostic Pitfalls, and a Unified Clinical Algorithm.Journal of clinical medicine · 2026Review
- Fuzzy boundaries between physical and emotional triggers in Takotsubo syndrome: a scoping review.BMC cardiovascular disorders · 2026Article
- Oxidative Stress in Takotsubo Syndrome: Insights into Extracellular Vesicles and Their Potential Clinical Relevance.Antioxidants (Basel, Switzerland) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Takotsubo syndrome (TTS) is a clinical condition characterized by left ventricular dysfunction, clinically mimicking acute coronary syndrome. Despite significant advancements in understanding TTS, more questions about its underlying pathological mechanisms remain unresolved. The present review offered current data on the underlying pathological mechanisms of TTS, including central nervous system structural and functional alterations, sympathetic nervous system overstimulation, excessive catecholamine secretion, shifts in adrenergic receptors (ARs) distribution and balance, hormone influences, epicardial vasospasm, endothelial dysfunction and genetic predispositions. For example, stressors from physical or emotional triggers induce central neurohumoral activation by influencing the hippocampus and amygdala, which results in excessive local or systemic secretion. This catecholamine surge affects the myocardium by altering cellular metabolism, disrupting signaling pathways and impairing endothelial function. The regional myocardial effects are influenced by the modified ARs distribution and the density of autonomic innervation, which are pivotal in the onset of TTS. These insights suggest potential therapeutic strategies, including cognitive behavioral therapy, endothelin A antagonists and β‑blockers. However, the complex interplay of these factors in TTS onset remains poorly understood. Further research is essential to elucidate the intricate mechanisms and interactions underlying this syndrome, paving the way for improved prevention and treatment approaches.
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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.