Pain Neuroscience and Organ Protection: Molecular Mechanisms

Pain and organ injury are linked through bidirectional neural and immune signaling. Peripheral nociceptors do not merely transmit noxious information: through neuropeptides, ion channels, trophic factors, and neuroimmune interactions, they can shape local inflammation, vascular tone, epithelial integrity, and tissue repair. Conversely, ischemia, inflammation, infection, and sterile tissue injury generate molecular signals that sensitize sensory pathways and promote persistent pain. Recent advances in single-cell and spatial omics, cell-specific genetic manipulation, neural circuit tools, and organoid and co-culture systems now permit dissection of these interactions at molecular and cellular resolution. However, the mechanistic links connecting nociceptor activity, glial and immune responses, and organ protection or maladaptation remain fragmented across organ systems.This Research Topic aims to define how molecular processes in pain-relevant neural systems influence organ injury, protection, and repair, and how organ-derived signals reshape nociceptive processing. The central challenge is to move beyond descriptive associations between pain and systemic disease by identifying causal cellular and molecular pathways. We seek studies that integrate sensory neurons, autonomic pathways, glia, immune cells, and target-organ cells using rigorous mechanistic approaches. By bringing together work across neurological and peripheral organ contexts, the collection will identify shared neuroimmune principles, clarify context-specific mechanisms, and highlight experimentally tractable targets for protecting organs while limiting maladaptive pain signaling.We welcome original research, systematic reviews, and focused perspectives that provide molecular or cellular mechanistic insight. Clinical observational studies without mechanistic readouts are outside the scope. Relevant themes include:• Nociceptor, dorsal root ganglion, and autonomic regulation of organ injury and repair• Neuropeptides, ion channels, and receptor signaling at neuroimmune interfaces• Glial, macrophage, mast-cell, and lymphocyte interactions with sensory neurons• Molecular mechanisms linking ischemia-reperfusion, inflammation, or fibrosis to pain sensitization• Bidirectional neural-organ communication in the kidney, liver, heart, lung, gut, and brain• Single-cell, spatial, genetic, and functional approaches that establish causal mechanisms Topic editors: Dai-Qiang Liu, Ya-Qun Zhou, Fu-Chao Zhang Source: https://www.frontiersin.org/research-topics/86231/pain-neuroscience-and-organ-protection-molecular-mechanisms