Senescence-like states in dorsal root ganglion neurons and the failure of pain to resolve

Pain usually resolves as tissue inflammation subsides and sensory pathways return toward their pre-injury operating range. In some patients, nociceptive output persists after the initial lesion has stabilized. This Mini Review examines whether a durable senescence-like state in dorsal root ganglion (DRG) sensory neurons may contribute to failed pain resolution. We searched PubMed, Web of Science, and Scopus for English-language articles published from January 2016 to July 2026. Earlier mechanistic studies were included when they informed the central concepts. We prioritized original studies that identified the relevant cell type, assessed multiple senescence-associated features, incorporated temporal or functional measurements, or tested reversibility. Evidence from glia and peripheral tissues was included only when it clarified the neuronal hypothesis. Aging and nerve injury are associated with senescence-like features in subsets of mouse DRG neurons. The strongest direct evidence combines multiple markers with altered firing and behavioral improvement after senolytic treatment, although the intervention was not neuron-specific. Single-cell studies identify senescence-associated transcriptional programs in nociceptor subsets. Studies of persistent excitability, local neuron-glia signaling, and mitochondrial dysfunction provide candidate links to failed pain resolution, but do not establish neuronal senescence as their cause. Senescence-like DRG neurons should be regarded as a testable contributor to failed pain resolution, not an established cause of chronic pain. Longitudinal studies must connect a composite neuronal state to sensory output, recovery trajectories, and selective reversal. Defined perioperative injuries provide a particularly observable model in which the timing of injury and divergence of recovery can be followed prospectively.