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Ventricular arrhythmias (VAs) after myocardial infarction (MI) are still one of the most important causes of cardiovascular death, though patients receive timely vascular recanalization and drug treatment. And it requires further exploring the mechanism and new therapeutics of VAs induced by MI. Here, we review the electrophysiological and neuroimmune mechanisms of VAs induced by MI. Immune cells are regulated by combining with neuroendocrine molecules released by the sympathetic nervous system (SNS), and, in turn, they modulate SNS both at the paraventricular nucleus of the hypothalamus and stellate ganglion by releasing cytokines or chemokines. In addition, 'life essentials' such as sleep, physiological health, and exercise can also influence cardiovascular health through neuroimmune mechanisms. Those factors and mechanisms provide us with new perspectives for understanding the occurrence and maintenance of VAs after MI. Exploring the crosstalk between electrophysiology and neuroimmunology will contribute to finding new therapeutics for VAs after MI.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12189811 | PMC |
http://dx.doi.org/10.3390/biomedicines13061290 | DOI Listing |
Immunity
September 2025
Institute for Infection Control and Prevention, Medical Center and Faculty of Medicine, University of Freiburg, Freiburg, Germany; Centre for Integrative Biological Signalling Studies (CIBSS), University of Freiburg, Freiburg, Germany; Center for Chronic Immunodeficiency (CCI), Medical Center and Fa
Resident macrophages play integral roles in maintaining tissue homeostasis and function. In the skin, prenatally seeded, specialized macrophages patrol sensory nerves and contribute to their regeneration after injury. However, mechanisms underlying the long-lasting postnatal commitment of these nerve-associated macrophages remain largely elusive.
View Article and Find Full Text PDFJ Neuroimmunol
August 2025
Department of Neuroscience, College of Medicine, University of Florida, Gainesville, FL, USA. Electronic address:
Methamphetamine use disorder remains a significant public health concern, impacting neuronal function, immune responses, and vascular integrity. Of particular interest is methamphetamine's disruption of the blood-brain barrier (BBB), a key event that triggers neuroimmune dysfunction and the development of neurodegenerative conditions. While the systemic effects of methamphetamine are well-characterized, the mechanism(s) governing its dysregulation of BBB physiology remain poorly understood.
View Article and Find Full Text PDFInt Immunopharmacol
September 2025
Hebei Medical University Postdoctoral Research Station in Basic Medicine, No. 361 Zhongshan Dong Road, 050017 Shijiazhuang, China; Hebei Key Laboratory of Forensic Medicine, Collaborative Innovation Center of Forensic Medical Molecular Identification, College of Forensic Medicine, Hebei Medical Univ
Environmental stress contributes to the development of depression through neuro-immune interactions, yet the underlying molecular mechanisms and associated clinical diagnostic biomarkers remain unclear. We established a psychosocial stress mouse model and systematically investigated the immune dysregulation induced by stress through integrated analysis of blood cell profiles, leukocyte transcriptomics, protein-protein interaction networks, single-cell RNA sequencing, and targeted pharmacological intervention. Additionally, we constructed and validated a depression predictive model using multiparametric peripheral blood data and machine learning, and assessed feature importance using the SHapley Additive exPlanations (SHAP) analysis.
View Article and Find Full Text PDFEndometriosis is a chronic, systemic, inflammatory disease characterized by the presence of endometrium-like tissue growing outside of the uterus. One of its main symptoms is chronic pain and inflammation leading to a decreased quality of life. This is a common disease, as at least one in ten female-born individuals have endometriosis.
View Article and Find Full Text PDFFront Immunol
September 2025
Department of Pharmacy, Shenzhen Longhua District Central Hospital, Shenzhen, China.
The immune interactions within the gut-brain axis represent a critical etiological factor in psychiatric disorders. The gut microbiota and their metabolites serve as biological mediators that regulate neuroimmune activation and suppression in the central nervous system (CNS). During intestinal immune activation, pro-inflammatory cytokines (, IL-6, TNF-α) propagate to the CNS compromised blood-brain barrier (BBB) integrity or vagal afferent fibers, disrupting neurotransmitter metabolism and inducing microglial hyperactivation, thereby exacerbating neuroinflammation.
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