IL-1 / emergency myelopoiesis is upstream of aged HSC bias, but not yet a universal longevity bottleneck

IL-1 / emergency myelopoiesis is upstream of aged HSC bias, but not yet a universal longevity bottleneck ''结论'': IL-1 signaling can clearly drive aging-associated hematopoietic reprogramming: continuous low-level IL-1 contributes to HSPC functional decline, myeloid skew, CH expansion, and emergency myelopoiesis. However, the evidence base still clusters around marrow/HSPC phenotypes and cancer-promoting inflammation, not organism-level healthspan or lifespan rescue. ''筛选判断'': If a candidate strongly explains hematopoietic aging yet lacks direct lifespan/healthspan endpoints, it should remain a high-priority immune upstream entry but not be promoted above nodes with stronger organism-level evidence (for example IL-11). ''代表性线索'': PMID 36379023 (Aging drives Tet2+/- clonal hematopoiesis via IL-1 signaling); PMID 38781562 (IL-1 in aging and pathologies of hematopoietic stem cells); Science 2024 on hematopoietic aging promoting cancer via IL-1α-driven emergency myelopoiesis.