IL-1 is a strong upstream hematopoietic inflammaging loop, but not yet a universal longevity bottleneck
fact lesson principle aging immunology
IL-1 is a strong upstream hematopoietic inflammaging loop, but not yet a universal longevity bottleneck
''结论'': IL-1 signaling clearly sits upstream of aged HSC bias, microbiome-driven inflammaging, and Tet2+/− clonal hematopoiesis; however, the public evidence still does **not** show organism-level lifespan/healthspan improvement comparable to the strongest longevity candidates.
''关键原始证据'':
# PMID 34525198 / IL-1 mediates microbiome-induced inflammaging of hematopoietic stem cells in mice: IL-1 mediates microbiome-induced inflammaging of HSCs.
# PMID 36379023 / Aging drives Tet2+/- clonal hematopoiesis via IL-1 signaling: aging promotes Tet2+/− clonal hematopoiesis through IL-1 signaling.
# PMID 30988118 / Trauma Induces Emergency Hematopoiesis through IL-1/MyD88-Dependent Production of G-CSF: IL-1/MyD88 can drive emergency hematopoiesis.
# PMID 25114230 / Interleukin-1 deficiency prolongs ovarian lifespan in mice: IL-1 loss prolongs ovarian lifespan, but this is tissue-specific rather than whole-organism longevity evidence.
''可复用判断'': 当一个炎症轴主要证明为 HSC/髓系偏倚的上游驱动，而缺少全身 lifespan / multi-organ healthspan 终点时，它应被视为“高杠杆上游回路”，但还不能自动升级为“通用长寿瓶颈”。