ArticleJournal of cellular and molecular medicine2013
Vagal nerve stimulation protects cardiac injury by attenuating mitochondrial dysfunction in a murine burn injury model.
Article in Journal of cellular and molecular medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- Use of 1H-nuclear magnetic resonance to screen a set of biomarkers for monitoring metabolic disturbances in severe burn patients.Critical care (London, England) · 2014Trial
- Mitochondria as a Therapeutic Target for Burn Injury.Biomolecules · 2026Review
- Electrical Vagus Nerve Stimulation Ameliorates Cardiac Ischemia and Reperfusion Injury by Improving Mitochondrial Biogenesis Through the SIRT1/PGC-1α Pathway.Applied biochemistry and biotechnology · 2025Article
- Role of oxidative stress in post-burn wound healing.Burns & trauma · 2025Review
- Neuron-Microglia Interaction is Involved in Anti-inflammatory Response by Vagus Nerve Stimulation in the Prefrontal Cortex of Rats Injected with Polyinosinic:Polycytidylic Acid.Molecular neurobiology · 2024Article
- Vagal nerve stimulation in myocardial ischemia/reperfusion injury: from bench to bedside.Bioelectronic medicine · 2024Review
- Research progress on the improvement of cardiovascular diseases through the autonomic nervous system regulation of the NLRP3 inflammasome pathway.Frontiers in cardiovascular medicine · 2024Review
- Article
- Vagus Nerve Stimulation and Its Cardioprotective Abilities: A Systematic Review.Journal of clinical medicine · 2023Review
- Pathological Responses of Cardiac Mitochondria to Burn Trauma.International journal of molecular sciences · 2020Review
- Intraoperative Vagus Nerve Stimulation Accelerates Postoperative Recovery in Rats.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2019Article
- Phoenixin-14: detection and novel physiological implications in cardiac modulation and cardioprotection.Cellular and molecular life sciences : CMLS · 2018Article
- Burn Serum Stimulates Myoblast Cell Death Associated with IL-6-Induced Mitochondrial Fragmentation.Shock (Augusta, Ga.) · 2017Article
- Vagal nerve stimulation improves mitochondrial dynamics via an MJournal of cellular and molecular medicine · 2017Article
- Cardiovascular Dysfunction Following Burn Injury: What We Have Learned from Rat and Mouse Models.International journal of molecular sciences · 2016Review
- Notch1 Pathway Protects against Burn-Induced Myocardial Injury by Repressing Reactive Oxygen Species Production through JAK2/STAT3 Signaling.Oxidative medicine and cellular longevity · 2016Article
- Novel strategies and underlying protective mechanisms of modulation of vagal activity in cardiovascular diseases.British journal of pharmacology · 2015Review
- Effect of the M1 Muscarinic Acetylcholine Receptor on Retinal Neuron Number Studied with Gene-Targeted Mice.Journal of molecular neuroscience : MN · 2015Article
- Article
- Membrane potential-dependent uptake of 18F-triphenylphosphonium--a new voltage sensor as an imaging agent for detecting burn-induced apoptosis.The Journal of surgical research · 2014Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondria play a central role in the integration and execution of a wide variety of apoptotic signals. In the present study, we examined the deleterious effects of burn injury on heart tissue. We explored the effects of vagal nerve stimulation (VNS) on cardiac injury in a murine burn injury model, with a focus on the protective effect of VNS on mitochondrial dysfunction in heart tissue. Mice were subjected to a 30% total body surface area, full-thickness steam burn followed by right cervical VNS for 10 min. and compared to burn alone. A separate group of mice were treated with the M3-muscarinic acetylcholine receptor (M3-AchR) antagonist 4-DAMP or phosphatidylinositol 3 Kinase (PI3K) inhibitor LY294002 prior to burn and VNS. Heart tissue samples were collected at 6 and 24 hrs after injury to measure changes in apoptotic signalling pathways. Burn injury caused significant cardiac pathological changes, cardiomyocyte apoptosis, mitochondrial swelling and decrease in myocardial ATP content at 6 and 24 hrs after injury. These changes were significantly attenuated by VNS. VNS inhibited release of pro-apoptotic protein cytochrome C and apoptosis-inducing factor from mitochondria to cytosol by increasing the expression of Bcl-2, and the phosphorylation level of Bad (pBad(136)) and Akt (pAkt(308)). These protective changes were blocked by 4-DAMP or LY294002. We demonstrated that VNS protected against burn injury-induced cardiac injury by attenuating mitochondria dysfunction, likely through the M3-AchR and the PI3K/Akt signalling pathways.
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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.