ArticleCardiovascular drugs and therapy2026
Vagus Nerve Stimulation by Focused Ultrasound Attenuates Acute Myocardial Ischemia/Reperfusion Injury Predominantly Through Cholinergic Anti-inflammatory Pathway.
Article in Cardiovascular drugs and therapy, 2026. 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
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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
3 citing papers in PubMed.
- Beyond cardiac fibroblasts: research advances on understanding and targeting intercellular communication networks in cardiac fibrosis.Frontiers in cardiovascular medicine · 2026Review
- Bidirectional brain-heart communication in coronary heart disease: from coronary plaques to central autonomic networks.Frontiers in neuroscience · 2026Review
- Ultrasound stimulation of the vagus nerve as a treatment modality for anxiety.Frontiers in psychiatry · 2024Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
purposeThis study investigates the cardioprotective effects of focused ultrasound stimulation (FUS) as a novel, noninvasive intervention for mitigating acute myocardial ischemia/reperfusion (I/R) injury.
methodsIn rat I/R models (30-min left anterior descending coronary artery (LAD) occlusion followed by 2-/24-h reperfusion), FUS was applied to the right cervical vagus nerve during early reperfusion (10-60 min post-reperfusion). The effects of FUS were assessed by analyzing inflammatory markers, arrhythmia incidence, pathological changes, echocardiographic parameters, pro-/anti-oxidative biomarkers, myocardial fibrosis, and infarct size. To elucidate the underlying mechanism, vagotomy and atropine administration were performed.
resultsFUS significantly reduced heart rate and inflammation in the 2-h reperfusion model. Compared to the I/R group, the I/R + FUS group exhibited markedly decreased premature ventricular contractions (221.00 ± 166.93 vs 83.11 ± 34.08, p < 0.05), ventricular tachycardia and ventricular fibrillation (16.67 ± 10.68 vs. 3.67 ± 3.24, p < 0.01), and arrhythmia scores during reperfusion (2.44 ± 1.13 vs. 0.67 ± 0.50, p < 0.01). In the 24-h reperfusion model, FUS significantly reduced myocardial fibrosis and infarct size (infarct size/area at risk 49.60 ± 9.17% vs. 20.73 ± 4.91%, p < 0.001) and preserved left ventricular ejection fraction (35.68 ± 9.95% vs 56.73 ± 2.64%, p < 0.001). The protective effects of FUS were abolished by vagotomy or atropine, suggesting the cholinergic anti-inflammatory pathway as a potential mechanism.
conclusionTargeted FUS neuromodulation exerts acute and sustained cardioprotection against I/R injury primarily through cholinergic anti-inflammatory mechanisms, offering a safer and more accessible alternative to traditional treatments.
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