The Brain–Body Interplay in Pain, Anesthesia, and Oncology

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 31 December 2026 | Viewed by 2665

Editor

Department of Anesthesiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
Interests: anesthesia

Special Issue Information

Dear Colleagues,

This Special Issue focuses on how signals between the nervous system and peripheral organs shape pain, responses to anesthetic drugs, and cancer biology and outcomes. We welcome studies across basic, translational, and clinical domains that clarify mechanisms and identify measurable targets. Microbiome-related pathways are examples of interest—such as the gut–brain, gut–lung, and gut–liver axes—together with neuroimmune, neuroendocrine, autonomic, and metabolic links that connect the periphery with central circuits. Relevant topics include how microbial metabolites, systemic inflammation, and host metabolism influence nociception and central processing; how anesthetic exposure and depth affect neurocognition and neuroinflammation; and how brain–body communication shapes tumor behavior, immune competence, treatment tolerance, and symptom burden. We encourage work that integrates preclinical and clinical models, employs methods such as multi-omics, imaging, and electrophysiology, and uses sound designs capable of supporting causal interpretation. Submissions may address mechanisms, biomarkers, and interventions (e.g., microbiome-directed, neuromodulatory, or metabolic). The goal is to define concrete pathways and measures that can guide research and practice across pain, anesthesia, and oncology.

Dr. Hui Xu
Guest Editor

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Keywords

  • brain–body axis
  • neuroimmune communication
  • microbiome–gut–brain axis
  • nociception
  • anesthetic outcomes
  • cancer biology

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Published Papers (3 papers)

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Research

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19 pages, 13983 KB  
Article
Sevoflurane-Associated Plasma Extracellular Vesicles Promote Aggressive Phenotypes in Cervical Cancer Cells with Concurrent DG Remodeling and EGFR/PKCα/NF-κB Activation
by Bo Jiao, Danning Wang, Jia Wei, Shaodi Guan, Yali Li, Yun Liu, Shaomeng Si, Yueyang Xin, Jie Dong, Siqi Zhou, Pei Lu and Hui Xu
Biomedicines 2026, 14(6), 1333; https://doi.org/10.3390/biomedicines14061333 - 12 Jun 2026
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Abstract
Background/Objectives: Whether anesthetic maintenance influences tumor biology in cervical cancer remains unsettled. We examined whether plasma extracellular vesicles (EVs) collected during sevoflurane or propofol anesthesia differentially affect HeLa cell behavior and explored lipidomic alterations associated with the biologically active EV condition. Methods [...] Read more.
Background/Objectives: Whether anesthetic maintenance influences tumor biology in cervical cancer remains unsettled. We examined whether plasma extracellular vesicles (EVs) collected during sevoflurane or propofol anesthesia differentially affect HeLa cell behavior and explored lipidomic alterations associated with the biologically active EV condition. Methods: In a single-center prospective observational cohort, paired plasma samples were collected before anesthesia induction and before wound closure from 53 patients with stage II cervical cancer undergoing radical surgery under sevoflurane (n = 28) or propofol (n = 25) anesthesia. EV preparations were characterized by transmission electron microscopy, nanoparticle tracking analysis, and immunoblotting for EV markers. Their effects on HeLa cell proliferation, invasion, and wound closure, as well as HUVEC tube formation, were examined in vitro. EV miRNA profiles were analyzed by small-RNA sequencing. Lipidomic profiling by LC-MS and immunoblot analysis of EGFR/PKCα/NF-κB signaling were performed in recipient HeLa cells exposed to sevoflurane-associated EVs. Results: EVs collected after sevoflurane anesthesia increased HeLa cell proliferation, invasion, and wound closure and enhanced endothelial branching in HUVEC tube-formation assays, whereas post-propofol EVs showed no comparable phenotype. Small-RNA sequencing identified distinct anesthesia-associated EV miRNA changes, with the sevoflurane-related signature enriched in glycerolipid metabolism, glycerophospholipid metabolism, glycosylphosphatidylinositol-anchor biosynthesis, phosphatidylinositol signaling, and inositol phosphate metabolism. In HeLa cells treated with post-sevoflurane EVs, lipidomic analysis showed clear separation from pre-sevoflurane EV-treated cells and identified increased diacylglycerol (DG) species, including DG (16:1/18:2), DG (16:0/16:1), DG (18:2/18:2), DG (18:2/20:4), and DG (16:0/18:2). These changes were accompanied by higher p-EGFR, PKCα, and p-NF-κB p65 levels. Several DG species correlated positively with proliferation and invasion readouts and inversely with residual wound area. Conclusions: Plasma EVs collected after sevoflurane anesthesia were associated with a more aggressive phenotype in recipient cervical cancer cells and with lipid remodeling characterized by DG accumulation and altered EGFR/PKCα/NF-κB signaling. The data support an exploratory mechanistic model linking sevoflurane-associated EV cargo to metabolic reprogramming in cervical cancer cells. Full article
(This article belongs to the Special Issue The Brain–Body Interplay in Pain, Anesthesia, and Oncology)
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Review

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16 pages, 1880 KB  
Review
Targeting CRMP2 for Chronic Pain: From Molecular Mechanisms to Therapeutic Strategies
by Jia-Yi Wang, Dai-Qiang Liu, Ya-Qun Zhou and Wei Mei
Biomedicines 2026, 14(7), 1512; https://doi.org/10.3390/biomedicines14071512 - 5 Jul 2026
Abstract
Collapsin Response Mediator Protein 2 (CRMP2) has emerged as a central node in the pathogenesis of chronic pain, functioning as a multimodal ‘molecular switch’ that regulates microtubule dynamics, ion channel trafficking, and synaptic plasticity. The dysregulation of CRMP2, particularly through aberrant post-translational modifications [...] Read more.
Collapsin Response Mediator Protein 2 (CRMP2) has emerged as a central node in the pathogenesis of chronic pain, functioning as a multimodal ‘molecular switch’ that regulates microtubule dynamics, ion channel trafficking, and synaptic plasticity. The dysregulation of CRMP2, particularly through aberrant post-translational modifications (PTMs) such as phosphorylation and SUMOylation, is a critical driver of both peripheral and central sensitization. This review systematically examines the structure, regulation, and multifaceted roles of CRMP2 in pain signaling pathways. We then critically evaluate a spectrum of CRMP2-targeted therapeutic strategies, including small-molecule inhibitors, peptide-based agents, and gene silencing, highlighting their promising preclinical efficacy and safety profiles. Despite challenges in targeting specificity and central nervous system delivery, we posit that innovations in delivery systems, precision medicine, and AI-assisted drug design will catalyze the clinical translation of CRMP2-based, non-opioid analgesics, offering a paradigm shift in chronic pain management. Full article
(This article belongs to the Special Issue The Brain–Body Interplay in Pain, Anesthesia, and Oncology)
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24 pages, 1822 KB  
Review
Adipose Tissue and Central Nervous System Crosstalk: Roles in Pain and Cognitive Dysfunction
by Juan Li, Zhixiao Li, Kun Chen, Yanqiong Wu, Xuesong Yang, Zhigang He and Hongbing Xiang
Biomedicines 2026, 14(1), 54; https://doi.org/10.3390/biomedicines14010054 - 26 Dec 2025
Cited by 5 | Viewed by 1882
Abstract
The global obesity pandemic has unveiled adipose tissue as a pivotal, active modulator of neurological health, intricately linking metabolic dysfunction to chronic pain and cognitive decline. This review synthesizes current evidence to propose a unified “neuro-metabo-inflammatory” model of the adipose-central nervous system (CNS) [...] Read more.
The global obesity pandemic has unveiled adipose tissue as a pivotal, active modulator of neurological health, intricately linking metabolic dysfunction to chronic pain and cognitive decline. This review synthesizes current evidence to propose a unified “neuro-metabo-inflammatory” model of the adipose-central nervous system (CNS) axis. We articulate a framework where, in pathological states such as obesity, dysfunctional adipose tissue releases a milieu of factors—including adipokines, lipids, and extracellular vesicles—that propagate peripheral and central neuroinflammation, disrupt blood–brain barrier integrity, and impair synaptic plasticity. These processes converge to drive pain sensitization and cognitive deficits. Critically, we evaluate the clinical evidence linking visceral adiposity to multisite chronic pain and accelerated cognitive impairment, while highlighting sexually dimorphic pathways. The review moves beyond cataloging findings to prioritize the most robust mechanisms, assess evidence quality, and identify key translational gaps. We conclude by discussing emerging therapeutic strategies targeting this axis and proposing precise directions for future research to disentangle the complex temporal and spatial dynamics of adipose–CNS communication. Full article
(This article belongs to the Special Issue The Brain–Body Interplay in Pain, Anesthesia, and Oncology)
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