Aging-linked ETS1-MYO1B vascular niche in human skin and ipragliflozin in aged rats
In this abstract, a machine-learning single-cell age clock built from published human skin data identified an aging-associated pericyte subcluster marked by MYO1B and an endothelial-to-pericyte transition; ipragliflozin suppressed the ETS1-MYO1B axis in vitro and in a D-galactose aging rat model. [1]
Automatic summary · not editorially reviewed
The key findings
A machine-learning single-cell age clock built from three published human skin single-cell transcriptomic datasets correlated with chronological age, and endothelial cells, lymphatic endothelial cells and pericytes carried the strongest aging signals. [1]
An aging-associated pericyte subcluster marked by MYO1B and a continuous endothelial-to-pericyte transition were identified, and TGF-β1/IL-1β stimulation induced MYO1B- and PDGFRB-positive pericyte-like transition and senescence in HMEC-1 cells. [1]
Ipragliflozin bound the transcription-regulatory region of ETS1, suppressed the ETS1-MYO1B axis and reduced EndoPT and senescence in vitro, and in aged rat skin restored epidermal thickness while reducing MYO1B, PDGFRB and PAI-1. [1]
The source at a glance
- Study type / format
- Abstract of a multimodal preclinical and observational study
- Population / context
- Published human skin single-cell transcriptomic datasets, 15 human skin samples, HMEC-1 cells and D-galactose-induced aging rats.
- Summary based on
- Study abstract
- Original publication
- September 25, 2026
Human skin single-cell age clock and validation
The authors built a machine-learning single-cell age-clock model from three published human skin single-cell transcriptomic datasets and checked it against chronological age; predicted age correlated with chronological age. Endothelial cells, lymphatic endothelial cells and pericytes carried the strongest aging signals. Findings were further checked in 15 human skin samples using H&E-based digital image analysis and immunohistochemistry. Aged skin showed a higher low-hematoxylin-area burden, reduced boundary-complexity variation and reduced vascular-area heterogeneity.
Supporting source [1]
MYO1B pericyte subcluster and EndoPT in vitro
Vascular subpopulations were resolved by NMF clustering and diffusion pseudotime analysis. The authors identified an aging-associated pericyte subcluster marked by MYO1B, together with a continuous endothelial-to-pericyte transition (EndoPT). In an inflammatory HMEC-1 model, TGF-β1/IL-1β stimulation induced MYO1B- and PDGFRB-positive pericyte-like transition and senescence. ETS1 bound the MYO1B promoter and was associated with aging status.
Supporting source [1]
Ipragliflozin effects in vitro and in aged rats
Structure-based virtual screening of an FDA drug library, molecular dynamics simulation and biolayer interferometry were used to identify and validate ETS1-targeting compounds. Ipragliflozin bound the transcription-regulatory region of ETS1, suppressed the ETS1-MYO1B axis, reduced EndoPT and senescence in vitro, and restored epidermal thickness while reducing MYO1B, PDGFRB and PAI-1 in aged rat skin. Efficacy was assessed in vivo in a D-galactose-induced aging model treated with oral ipragliflozin.
Supporting source [1]
How to interpret this
This explainer is based only on the abstract; the full text was not reviewed. The abstract reports no sample sizes for the three published datasets, no effect sizes or confidence intervals, and no details on randomization, blinding or controls in the rat experiment. The human analyses are observational associations, not causal evidence. The in vitro work used an inflammatory HMEC-1 cell model, and the in vivo efficacy was tested in a D-galactose-induced aging rat model, so the findings do not establish human lifespan or disease benefits.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Jin M, Zhang Y, Wu H, You B, Li L, Han X, Wu Y. · europepmc.org · September 25, 2026