Mouse Interleukin-1 Alpha (IL-1α) is a pro-inflammatory cytokine belonging to the IL-1 family—which includes IL-1α, IL-1β, and the IL-1 receptor antagonist (IL-1Ra)—and plays a central role in initiating innate and sterile inflammatory responses in mice (Mus musculus). IL-1α is constitutively expressed in epithelial, endothelial, and barrier tissues and functions as an intracellular alarmin that is rapidly released upon cell injury, necrosis, or cellular stress, independent of inflammasome processing. Upon binding to the IL-1 receptor type 1 (IL-1R1), murine IL-1α activates NF-κB and MAPK signaling pathways that promote leukocyte recruitment, endothelial activation, fever, and amplification of downstream pro-inflammatory cytokine cascades. Mouse IL-1α is widely studied in experimental models of sterile inflammation, ischemia–reperfusion injury, atherosclerosis, cancer-associated inflammation, inflammatory bowel disease, and autoimmune arthritis, where it contributes to early tissue inflammation and immune cell infiltration. IL-1α–deficient and IL-1R1 knockout mouse models have been instrumental in distinguishing inflammasome-independent inflammatory mechanisms from IL-1β–driven responses. As both a biomarker and therapeutic target, murine IL-1α remains central to preclinical research investigating cytokine-mediated pathology, tumor microenvironment dynamics, and development of IL-1–targeted anti-inflammatory strategies relevant to human inflammatory and autoimmune diseases.