#aging
- 重编程中的 senescence 可能是阶段依赖而非单向有害 20260425170201000
- 单一组织内 senescence 负担态与生态位态的可证伪判别框架 20260425165902000
- ER stress UPR not yet baseline-positive as a mammalian longevity node 20260425154643000
- Heat-shock/chaperone augmentation is not yet baseline-positive as a mammalian longevity node 20260425154317000
- Proteasome augmentation is not yet baseline-positive as a longevity node 20260425154052000
- 不要把整类机制一刀切地排除 20260425153833000
- Mitochondrial interventions have direct lifespan-endpoint positives, but evidence is heterogeneous 20260425153808000
- Autophagy enhancement is not yet baseline-positive like rapamycin/mTOR 20260425153601000
- Rapamycin is a baseline-positive specific node; autophagy and mitochondria are not automatically longevity candidates 20260425153226000
- 候选筛选要用“干预 + 终点”双约束检索 20260425152851000
- mTOR/rapamycin 优先于泛化自噬/线粒体作为长寿候选 20260425152830000
- IL-11 的寿命/健康寿命效应大小与证据边界 20260425152333000
- IL-11 抑制的成年哺乳动物证据层级 20260425152029000
- IL-11 修复代价的直接成人哺乳动物原始反例仍未检出 20260425151726000
- Adult-mammal IL-11 inhibition: direct bone-homeostasis harm, fracture/wound evidence still missing 20260425151443000
- IL-11 longevity benefit must be decomposed into immune/inflammatory and tissue-tradeoff components 20260425150607000
- IL-11 currently ranks above other screened immune/inflammation axes because it has direct mammalian healthspan/lifespan evidence 20260425150330000
- 补体级联仍未跨过通用长寿瓶颈门槛 20260425150146000
- IL-1/MyD88 outranks TNF/IL-6 as an upstream screening candidate, but not as a universal bottleneck 20260425145846000
- Complement cascade remains a high-potential but not yet universal longevity bottleneck 20260425145530000
- TNF/IL-6 are low-priority control axes in longevity bottleneck screening 20260425145355000
- cGAS-STING is a strong but context-dependent aging node, not yet a universal longevity bottleneck 20260425145335000
- type I interferon / JAK-STAT is an upstream amplifier, not a default universal longevity bottleneck 20260425145224000
- Thymic source restoration is a strong immune upstream entry, but not yet a universal longevity bottleneck 20260425144604000
- TNF/IL-6 are context-specific inflammaging mediators, not universal longevity bottlenecks 20260425144110000
- cGAS-STING is an upstream inflammaging amplifier, but not yet a universal longevity bottleneck 20260425143829000
- NLRP3 is a strong aging node but still not clearly a universal longevity bottleneck 20260425143408000
- complement 轴是高潜力候选但尚非 universal longevity bottleneck 20260425143032000
- IL-11 longevity candidacy must be split by tissue-specific tradeoffs 20260425142558000
- IL-1 is a strong upstream hematopoietic inflammaging loop, but not yet a universal longevity bottleneck 20260425142133000
- IL-11 inhibition: bone-homeostasis evidence is direct, fracture-healing evidence remains missing 20260425135719000
- Adult-mammal IL-11 inhibition has clear bone-homeostasis consequences, but direct fracture/wound inhibition evidence is sparse 20260425135357000
- IL-11 still needs a pleiotropy tradeoff audit before universal-bottleneck promotion 20260425134905000
- IL-6 trans-signaling is a plausible inflammaging axis, but not a universal longevity bottleneck 20260425134712000
- IgG/FcRn is a strong immune age-amplifying axis, but not yet a universal longevity bottleneck 20260425134301000
- IL-1 outranks TNF and type I IFN as an upstream immune loop, but still falls short of a universal longevity bottleneck 20260425133745000
- IL-11 is a strong candidate but not yet a universal bottleneck 20260425133514000
- 反证优先于升级候选 20260425133423000
- IL-17 / Th17 is a context-dependent inflammaging axis, not a universal longevity bottleneck 20260425133233000
- IL-11 remains the current top immune/inflammation longevity candidate, but not yet a universal bottleneck 20260425132624000
- C1q brain aging mechanism is informative but still insufficient for universal longevity candidacy 20260425131714000
- 寿命终点优先于通路热度 20260425131208000
- IL-11 is currently the strongest immune/inflammation longevity candidate in the screening set 20260425131144000
- IgG is a strong age-amplifying node, but not yet a universal longevity bottleneck 20260425130909000
- Antibody / IgG accumulation is a strong age-amplifying node, but not yet a universal longevity bottleneck 20260425130643000
- trained immunity is a functional defense amplifier, not a higher-priority longevity bottleneck than thymic source restoration 20260425130412000
- IL-1 / emergency myelopoiesis is upstream of aged HSC bias, but not yet a universal longevity bottleneck 20260425125943000
- type I interferon / JAK-STAT chronic activation is strong but context-dependent, not yet a universal bottleneck 20260425125646000
- C1q is aging-associated but not yet a universal longevity bottleneck 20260425125313000
- IL-11 is a strong lifespan-positive inflammaging node, but still not yet a universal immune bottleneck 20260425124410000
- FGF21 不是通用免疫长寿瓶颈,而是局部胸腺 niche 入口 20260425123837000
- NLRP3 is context-dependent longevity-positive, not yet a universal bottleneck 20260425051109000
- 单组织寿命正例不足以把炎症轴抬升为通用长寿瓶颈 20260425050954000
- 按因果广度而不是表面上游性来排长寿瓶颈 20260425050740000
- HSC/髓系偏置尚不能压过胸腺源恢复的免疫长寿排序 20260425050727000
- 局部语境决定抗衰老信号是否成立 20260425050544000
- Source-restoration immune entries outrank peripheral T-cell quality control when only the former has healthspan extension 20260425050521000
- Mature T-cell quality control usually ranks below thymic source restoration as a longevity entry 20260425050406000
- 免疫长寿入口的上游性排序 20260425050322000
- 免疫长寿入口的上游性排序:补给源 > 外周质量控制 > 局部 niche 维护 20260425050257000
- Peripheral T-cell quality control can reach frailty, but not yet lifespan 20260425050159000
- Peripheral T-cell quality control can reach frailty, while thymic regeneration remains mainly immune-readout level 20260425044850000
- T-cell Bcl-xL is a concrete peripheral quality-control example, but still not a validated universal longevity bottleneck 20260425044154000
- Peripheral lymph node niche repair is a lower-rank immune rejuvenation entry than thymic regeneration 20260425043703000
- Peripheral lymph node niche is a reversible immune entry, but not yet higher-leverage than thymic involution 20260425043458000
- Thymic involution remains the strongest reversible immune entry, but not yet a validated longevity bottleneck 20260425042531000
- IL-1 emergency myelopoiesis is upstream but not yet validated as a longevity bottleneck 20260425042245000
- Trained immunity is not yet a validated longevity bottleneck 20260425042105000
- 把 inflammaging 当作回路读出而非单一瓶颈 20260425041935000
- Inflammaging is better treated as a heterogeneous readout than a universal upstream bottleneck 20260425041919000
- Thymus regeneration improves immune readouts but not yet lifespan evidence 20260425041751000
- Immune rejuvenation can improve systemic aging phenotypes via thymic or peripheral routes 20260425041629000
- Immune interventions can improve systemic aging phenotypes, but not always via thymic regeneration 20260425041447000
- Immune longevity candidate ranking: thymic involution first, readouts later 20260425041227000
- 优先寻找“可逆上游入口”而不是只看年龄读出 20260425041000000
- Thymic involution can be experimentally reversed to restore naive T-cell output in aged mice 20260425040945000
- Inflammaging 更应默认按 context-dependent readout 处理 20260425040831000
- Netrin-1 可作为老化骨髓 niche 的可逆上游杠杆 20260425040329000
- Blood-aging candidate ranking: HSC exhaustion over CHIP; cell competition as framework 20260425040156000
- 先把 cell competition 当作框架,而不是立刻当作靶点 20260425040109000
- cell competition is a generic tissue-level quality-control framework 20260425040057000
- 老化干预要先找反馈回路 20260425035910000
- Bone marrow niche rejuvenation can restore aged HSC fitness 20260425035840000
- 年龄相关克隆现象优先视为读出而非总瓶颈 20260425035640000
- CHIP 更适合作为 HSC aging 的读出而非单一上游瓶颈 20260425035624000
- CDKN2A-OSK 在皮肤创面中的 FOSL1/迁移信号更应默认按间接效应解释 20260425035159000
- CDKN2A-OSK 在人皮肤创面中的直接效应与微环境间接效应应分层判断 20260425034935000
- FOSL1 不能被当成 CDKN2A-OSK 直接驱动角质形成细胞迁移的证据 20260425034652000
- CDKN2A-OSK 在人皮肤伤口边缘更像编辑炎症/应激状态,而非直接的增殖开关 20260425034427000
- 重编程效应要拆成炎症编辑与增殖激活两条轴 20260425034206000
- partial reprogramming 在人皮肤修复中更像炎症/应激状态编辑,而非增殖开关 20260425034137000
- partial reprogramming 在皮肤修复中更像炎症/应激状态编辑 20260425033952000
- 把干预时窗对齐到修复亚阶段 20260425033646000
- human skin wound-healing roadmap cleanly separates acute-support and chronic-failure programs 20260425033600000
- chronic wound failure programs clarify which senescence states are pathological 20260425033027000
- acute skin wound healing contains distinct senescent subpopulations with opposite effects 20260425032856000
- acute cutaneous wound healing is a clear example of context-dependent senescence 20260425032612000
- senolysis 可能破坏有益的再生 niche 20260425032437000