ArticlePloS one2026
A damage-structured PDE model of stem cell hierarchies: The dual role of dedifferentiation in tissue homeostasis and aging.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- FTU-Seek: Foundation Model-Guided Hard-Negative Learning for Sparse Functional Tissue Unit Segmentation.Biomedicines · 2026Article
- Computational Oncology of Chemotaxis-Driven Tumour-Immune Spatial Patterning and Stability.Bioengineering (Basel, Switzerland) · 2026Article
- Beyond diagonal noise: A better predator-prey modeling framework with cross-covariance.PloS one · 2026Article
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3 authors.
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Abstract
Stem cells maintain tissue integrity through a balance of self-renewal, differentiation, and loss of function due to aging or stress. Recent studies demonstrate that the stem cell hierarchy is not fixed. Transit-amplifying or terminally differentiated cells can dedifferentiate back into stem-like states. Such plasticity supports regeneration but, when combined with damage accumulation, may also accelerate aging and increase cancer risk. Motivated by these findings, we develop a damage-structured PDE model of a two-compartment lineage consisting of stem and terminally differentiated cells. The model incorporates dedifferentiation, together with a nonlocal δ-function kernel partitioning scheme that conserves total damage and encodes biologically motivated asymmetries. Methodologically, we emphasize reproducibility and robustness on three fronts. First, the δ-kernel partitioning prevents the unbounded drift that arises in local models while preserving conservation. Second, a conservative finite-volume discretization with upwind fluxes and verified first-order accuracy ensures stability and exact mass balance, as confirmed by manufactured-solution tests. Third, distributional metrics and systematic parameter sweeps provide reproducible ways to quantify lineage-level damage dynamics under varying dedifferentiation and repair conditions. These analyses show that threshold-dependent and repair-modulated dedifferentiation both act as protective mechanisms: the former functions as a 'detoxification loop' that recycles high-damage cells, and the latter reduces the damage burden imported during dedifferentiation. Together, they mitigate aging-inducing effects. Parameter sweeps further delineate when dedifferentiation stabilizes tissue maintenance versus when it drives aging-like dynamics. Overall, our reproducible framework integrates biological insights on stem-cell plasticity and damage segregation with rigorous mathematical modeling, providing a foundation for experimental validation and therapeutic strategies targeting stem-cell aging and cancer initiation.
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