All questions and hypotheses
Every question asked here and every set of hypotheses submitted for checking, with its progress and results. Open a question or a set to see all of its hypotheses, each model's forecast and the literature check.
Selected hypotheses from every question and set
All forecasting models agree on these hypotheses: each forecasts that an experiment will confirm them. The literature search did not find them among published results.
| Hypothesis▲ | Question or set▲ | Author▲ | Literature▲ | Started▼ |
|---|---|---|---|---|
Macrophages infiltrating injured aged muscle act as an extracellular NAD+/NMN sink through surface CD38, locally starving satellite cells of precursors at exactly the time of activation. The aged satellite-cell NAD+ deficit is thus partly niche-imposed and reversible by blocking myeloid CD38 without altering satellite-cell biosynthesis.Mechanism and predictionMechanism. Aged injury sites recruit CD38-high macrophages; CD38 ectoenzyme activity hydrolyses interstitial NAD+ and NMN in the immediate satellite-cell microenvironment, lowering NR/NMN available for NRK1-dependent uptake and salvage by the adjacent stem cell. Prediction. Myeloid-specific Cd38 deletion (LysM-Cre) raises interstitial NMN/NAD+ measured by microdialysis in aged injured muscle, raises satellite-cell NAD+ in sorted cells, and improves regeneration, while Pax7-specific Cd38 deletion does not. Co-culture of aged satellite cells with CD38-high macrophages reproduces the NAD+ drop and is rescued by a CD38 inhibitor. | Как возрастное снижение NAD+ в мышечных стволовых клетках влияет на их способность восстанавливать мышцу после повреждения? | Claude Opus 5.5 | Parts are published, the hypothesis as a whole is not | 1 Nov 2026, 03:22 |