ArticleCellular and molecular life sciences : CMLS2022
Vagus nerve stimulation exerts cardioprotection against doxorubicin-induced cardiotoxicity through inhibition of programmed cell death pathways.
Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Transcutaneous auricular vagus nerve stimulation alleviates chronic heart failure by targeting cathepsin K/p53-mediated ferroptosis.Biology direct · 2026Article
- Key role of the autonomic nervous system in breast cancer (Review).Experimental and therapeutic medicine · 2026Review
- A Review of Vagus Nerve Stimulation for Disease: Comprehensive Theory and Evidence for Mechanisms of Action.Comprehensive physiology · 2026Review
- Mitochondrial homeostasis meets novel programmed cell death: crosstalk mechanisms underlying cardiovascular diseases progression.Cell communication and signaling : CCS · 2026Review
- Therapeutic potential of vagus nerve stimulation in neurodegenerative diseases: research progress and mechanisms.Frontiers in immunology · 2026Review
- The function of PCSK9 in doxorubicin-induced cardiotoxicity and its underlying mechanism.Scientific reports · 2025Article
- Multi-omics reveals the mechanism of vagus nerve stimulation in the treatment of chronic congestive heart failure.Scientific reports · 2025Article
- Research progress in myocardial function and diseases related to muscarinic acetylcholine receptor (Review).International journal of molecular medicine · 2025Review
- Vagus nerve stimulation alleviates myocardial injury following hepatic ischemia-reperfusion in rats by inhibiting ferroptosis via the activation of the SLC7A11/GPX4 axis.European journal of medical research · 2025Article
- Clinicopathological Studies on the Impact of Grape Seed Extract and L-Carnitine as Cardioprotective Agents Against Doxorubicin-Induced Toxicity in Rats.Life (Basel, Switzerland) · 2024Article
- Non-invasive vagus nerve stimulation in anti-inflammatory therapy: mechanistic insights and future perspectives.Frontiers in neuroscience · 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
- Magnetic vagus nerve stimulation alleviates myocardial ischemia-reperfusion injury by the inhibition of pyroptosis through the MJournal of nanobiotechnology · 2023Article
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Authors and funding
12 authors at 2 institutions in 1 country.
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Abstract
The aberration of programmed cell death including cell death associated with autophagy/mitophagy, apoptosis, necroptosis, pyroptosis, and ferroptosis can be observed in the development and progression of doxorubicin-induced cardiotoxicity (DIC). Vagus nerve stimulation (VNS) has been shown to exert cardioprotection against cardiomyocyte death through the release of the neurotransmitter acetylcholine (ACh) under a variety of pathological conditions. However, the roles of VNS and its underlying mechanisms against DIC have never been investigated. Forty adults male Wistar rats were divided into 5 experimental groups: (i) control without VNS (CSham) group, (ii) doxorubicin (3 mg/kg/day, i.p.) without VNS (DSham) group, (iii) doxorubicin + VNS (DVNS) group, (iv) doxorubicin + VNS + mAChR antagonist (atropine; 1 mg/kg/day, ip, DVNS + Atro) group, and (v) doxorubicin + VNS + nAChR antagonist (mecamylamine; 7.5 mg/kg/day, ip, DVNS + Mec) group. Our results showed that doxorubicin insult led to left ventricular (LV) dysfunction through impaired cardiac autonomic balance, decreased mitochondrial function, imbalanced mitochondrial dynamics, and exacerbated cardiomyocyte death including autophagy/mitophagy, apoptosis, necroptosis, pyroptosis, and ferroptosis. However, VNS treatment improved cardiac mitochondrial and autonomic functions, and suppressed excessive autophagy, apoptosis, necroptosis, pyroptosis, and ferroptosis, leading to improved LV function. Consistent with this, ACh effectively improved cell viability and suppressed cell cytotoxicity in doxorubicin-treated H9c2 cells. In contrast, either inhibitors of muscarinic (mAChR) or nicotinic acetylcholine receptor (nAChR) completely abrogated the favorable effects mediated by VNS and acetylcholine. These findings suggest that VNS exerts cardioprotective effects against doxorubicin-induced cardiomyocyte death via activation of both mAChR and nAChR.
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