Traumatic brain injury, spinal cord injury, and ischemic stroke share secondary pathological processes that may persist beyond the acute insult. Cellular senescence and senescence-like states may contribute to this persistence, but it remains unclear when injury-associated changes represent stable, harmful cell states rather than transient stress responses, and whether their causal relevance is comparable across diseases and cell types. This review compares evidence across cell types and disease stages to address these gaps and examine implications for biomarkers, patient selection, and treatment timing. Evidence strength is disease- and cell-type specific: traumatic brain injury is most consistently associated with chronic glial abnormalities; spinal cord injury provides the clearest mechanistic links among infiltrating macrophages, neurons, and the microvasculature; and ischemic stroke has stronger support in myeloid and neurovascular compartments than in neurons or astrocytes. We use the term senescence-injury axis as a comparative framework for the possibility that persistent injury-induced senescence-related states contribute to secondary tissue dysfunction. However, reliance on single markers, tissue-level associations, and non-cell-specific interventions limits causal inference. Establishing causality requires longitudinal, cell-resolved studies with temporally controlled, cell-specific manipulation, while translation requires biomarkers that identify a persistent, potentially modifiable target state. Overall, the senescence-injury axis is a disease- and cell-type-specific framework for testing mechanisms and guiding therapeutic development, rather than an established universal causal pathway.