ArticleCell death & disease2020
Vagus nerve stimulation optimized cardiomyocyte phenotype, sarcomere organization and energy metabolism in infarcted heart through FoxO3A-VEGF signaling.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Mechanisms of actin-binding proteins in glycolysis-cytoskeleton coupling.Journal of translational medicine · 2026Review
- Review
- Transcutaneous auricular vagus nerve stimulation alleviates chronic heart failure by targeting cathepsin K/p53-mediated ferroptosis.Biology direct · 2026Article
- A Review of Vagus Nerve Stimulation for Disease: Comprehensive Theory and Evidence for Mechanisms of Action.Comprehensive physiology · 2026Review
- Vagus Nerve Stimulation Attenuates Cognitive Impairment in Traumatic Brain Injury via the mtDNA/cGAS-STING/NLRP3 Inflammasome Axis.Neurocritical care · 2026Article
- Effects of transcutaneous auricular vagus nerve stimulation on cardiorespiratory fitness in patients with subacute stroke: a study protocol for a randomized controlled trial.Frontiers in cardiovascular medicine · 2026Article
- Therapeutic potential of vagus nerve stimulation in neurodegenerative diseases: research progress and mechanisms.Frontiers in immunology · 2026Review
- Brain‑heart axis: Neurostimulation techniques in ischemic heart disease (Review).International journal of molecular medicine · 2025Review
- Identifying Diagnostic Biomarkers for Electroacupuncture Treatment of Rheumatoid Arthritis Using Bioinformatic Analysis and Machine Learning Algorithms.Journal of pain research · 2025Article
- Ovarian aging: energy metabolism of oocytes.Journal of ovarian research · 2024Review
- VNS improves VSMC metabolism and arteriogenesis in infarcted hearts through m/n-AChR-Akt-SDF-1α in adult male rats.Journal of molecular histology · 2024Article
- Non-invasive vagus nerve stimulation in anti-inflammatory therapy: mechanistic insights and future perspectives.Frontiers in neuroscience · 2024Review
- Vagal Stimulation Ameliorates Non-Alcoholic Fatty Liver Disease in Rats.Biomedicines · 2023Article
- Vagus nerve stimulation-induced stromal cell-derived factor-l alpha participates in angiogenesis and repair of infarcted hearts.ESC heart failure · 2023Article
- Outcomes of hypothalamic oxytocin neuron-driven cardioprotection after acute myocardial infarction.Basic research in cardiology · 2023Article
- Genetic studies in the Pakistani population reveal novel associations with ventricular septal defects (VSDs).BMC pediatrics · 2023Article
- The protective effect of vagus nerve stimulation against myocardial ischemia/reperfusion injury: pooled review from preclinical studies.Frontiers in pharmacology · 2023Article
- Vagus nerve stimulation exerts cardioprotection against doxorubicin-induced cardiotoxicity through inhibition of programmed cell death pathways.Cellular and molecular life sciences : CMLS · 2022Article
- Study of variants associated with ventricular septal defects (VSDs) highlights the unique genetic structure of the Pakistani population.Italian journal of pediatrics · 2022Article
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vagus nerve stimulation (VNS) restores autonomic balance, suppresses inflammation action and minimizes cardiomyocyte injury. However, little knowledge is known about the VNS' role in cardiomyocyte phenotype, sarcomere organization, and energy metabolism of infarcted hearts. VNS in vivo and acetylcholine (ACh) in vitro optimized the levels of α/β-MHC and α-Actinin positive sarcomere organization in cardiomyocytes while reducing F-actin assembly of cardiomyocytes. Consistently, ACh improved glucose uptake while decreasing lipid deposition in myocytes, correlating both with the increase of Glut4 and CPT1α and the decrease of PDK4 in infarcted hearts in vivo and myocytes in vitro, attributing to improvement in both glycolysis by VEGF-A and lipid uptake by VEGF-B in response to Ach. This led to increased ATP levels accompanied by the repaired mitochondrial function and the decreased oxygen consumption. Functionally, VNS improved the left ventricular performance. In contrast, ACh-m/nAChR inhibitor or knockdown of VEGF-A/B by shRNA powerfully abrogated these effects mediated by VNS. On mechanism, ACh decreased the levels of nuclear translocation of FoxO3A in myocytes due to phosphorylation of FoxO3A by activating AKT. FoxO3A overexpression or knockdown could reverse the specific effects of ACh on the expression of VEGF-A/B, α/β-MHC, Glut4, and CPT1α, sarcomere organization, glucose uptake and ATP production. Taken together, VNS optimized cardiomyocytes sarcomere organization and energy metabolism to improve heart function of the infarcted heart during the process of delaying and/or blocking the switch from compensated hypertrophy to decompensated heart failure, which were associated with activation of both P13K/AKT-FoxO3A-VEGF-A/B signaling cascade.
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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 Socratic graph.