The existence of a single functional Sox2 allele in Sox2^EGFP mice imbalances the pool of dermal stem cells, generating an age-associated regenerative deficit in the skin. We hypothesized that these mice might thus present alterations in their cutaneous wound healing capacity during ageing. To test this hypothesis, we performed full-thickness splinted excisional wounds in the dorsal skin of aged (>19-month) and young (8-10 weeks) TR (Sox2^EGFP) mice and WT littermates. Differences in wound closure rates were found with ageing for WT and TR mice, but no differences were observed between genotypes. Morphometric analyses at day 10 post-wounding revealed non-significant differences between genotypes. Young TR mice presented higher wound bed cellularity than young WT mice, and old TR mice had decreased cellularity compared to young TR. Old TR group presented reduced leukocyte infiltration as compared to old WT, and young TR mice presented fewer CD206+ cells than young WT. Differences were also observed with ageing for both genotypes. Moreover, young animals presented higher collagen intensity levels than old ones, and differences were observed among genotypes. However, non-significant differences in collagen area and orientation were found. The expression levels of Col3a1 gene and genes involved in collagen synthesis were significantly reduced with ageing. Old TR mice presented fewer elastic fibres than old WT, but non-significant differences were observed in the mRNA levels of Fbn1, Mfap5, Eln and Fbln5 between genotypes. Altogether, our results demonstrate an age-associated regenerative dysfunction that is reinforced in some ECM-related aspects on Sox2-haploinsufficient mice.