Integrative Analysis Reveals a Key Role for CDKN1A in Impaired Wound Healing in Diabetic Patients
Summary: Original research in CCID (published Sept 4, 2025) combines single-cell transcriptomics with Mendelian randomization to implicate CDKN1A as a central inhibitor of proliferation and a driver of premature differentiation in non-healing diabetic wounds, with upstream regulation linked to FOS.
Key Highlights:
- scRNA-seq contrasts healing vs. non-healing DFUs and identifies CDKN1A upregulation in non-healing tissue.
- FOS emerges as a potential transcriptional regulator of CDKN1A in impaired healing.
- Mendelian randomization connects CDKN1A expression to metabolic signatures (e.g., α-ketobutyrate/pyruvate ratio) relevant to wound impairment.
- Targets in the FOS–CDKN1A axis are proposed as candidates for therapeutic modulation.
Keywords:
CDKN1A/p21,
FOS,
diabetic foot ulcer,
single-cell RNA-seq,
Mendelian randomization