ArticleBasic research in cardiology2025
The activation of catecholamine neurons in the rostral ventrolateral medulla drives ventricular remodeling after myocardial ischemia/reperfusion injury.
Article in Basic research in cardiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Spinal neuronal TLR4-induced enhancement of nociceptive signals contributes to myocardial ischemia/reperfusion injury.Basic research in cardiology · 2026Article
- The impact of primary percutaneous coronary intervention timing on prognosis in STEMI patients.Clinical medicine (London, England) · 2026Article
- The glutamatergic NTS-PAG/PVN pathway underlies myocardial injury and anxiety-like behavior induced by myocardial ischemia-reperfusion.Translational psychiatry · 2026Article
- Role of Exercise in Modulating the Brain-Heart Axis in Cardiovascular Diseases.International journal of molecular sciences · 2026Review
- Silk-Fibroin-Based Strategies for Myocardial Infarction Repair: A Comprehensive Review.International journal of molecular sciences · 2026Review
- Long-term social isolation during adolescence exacerbated cardiac dysfunction after myocardial infarction.Translational psychiatry · 2026Article
- Neural mechanism of HT7 electroacupuncture in myocardial ischemia: critical role of the paraventricular nucleus oxytocin system.Frontiers in neuroscience · 2025Article
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Authors and funding
17 authors.
Funding
Abstract
Catecholamine neurons in the rostral ventrolateral medulla (RVLM) have long been recognized as a crucial neuronal population involved in cardiovascular regulation. However, its function and related circuits in ventricular remodeling after myocardial ischemia/reperfusion injury (MIRI) remain unclear. In this study, we investigated the potential role of RVLM catecholaminergic neurons and the underlying mechanisms that drive MIRI and the development of post-MIRI ventricular remodeling. In vivo electrophysiological recordings revealed that the spontaneous spike rate of RVLM neurons increased throughout MIRI. Transneuronal tracing with neurotropic viruses indicated that the RVLM catecholaminergic neurons received glutamatergic projections from paraventricular nucleus (PVN). Specifically, these RVLM catecholaminergic neurons project directly to the spinal preganglionic neurons and then to the stellate ganglion, which are two critical neural nodes that regulate cardiovascular activity. In addition, inhibition of the neural circuit associated with RVLM catecholaminergic neurons suppresses cardiac sympathetic activity, thereby preventing MIRI and lessening the severity of ventricular remodeling at 4 weeks after MIRI. Our findings suggest that glutamatergic projections from PVN to RVLM catecholaminergic neurons are important yet distinctive mechanisms of the brain-to-heart axis in regulating MIRI and potentially mitigating ventricular remodeling and subsequent heart failure.
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Registered trials
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