Dermal fibroblast mitochondrial profiles in painful diabetic neuropathy
Authors' conclusion
Fibroblasts from participants with painful DPN did not differ in inflammatory and mitochondrial profiles compared with those from pain-free DPN. However, persistent dermal macrophage infiltration in painful DPN suggests a stable immune-activated microenvironment, potentially contributing to pain maintenance. Our results suggest that immune-related, rather than fibroblast-intrinsic, mechanisms could play a role in sustaining neuropathic pain in painful DPN.
Study context
- Population
- Participants with and without diabetes and diabetic polyneuropathy (DPN); dermal fibroblasts and skin biopsies24 fibroblast cultures
- Participants
- 30 participants
- Comparison
- Painful DPN vs pain-free DPN, diabetes without DPN and controls
- Controlsn = 5reference
- Diabetes without DPNn = 7
- Pain-free DPNn = 7
- Painful DPNn = 11
- Outcome
- Fibroblast and skin biopsy profiles
Main finding
As reported in the abstract
- Fibroblast morphology and proliferation did not differ significantly between groups
- No significant differences in fibroblast subtype distributions across groups
- Inflammatory mediator secretion was limited
- Mitochondrial mass, membrane potential, ROS production and bioenergetic parameters not different across groups
- Comparable fibroblast density and mitochondrial profiles in skin biopsies across groups
Further findings
| Outcome | Painful DPN | P value |
|---|---|---|
| Dermal macrophage infiltrationPainful DPN vs Controls · elevated with painful DPN | mean ≈8% | P = 0.02 |
| Dermal macrophage infiltrationPainful DPN vs Pain-free DPN | P = 0.07 |
- Dermal macrophage infiltration — Significantly elevated in painful DPN; ANOVA
- p=0.02
Langerhans cell area fraction
- Did not differ between groups
Original publication
Dermal fibroblast mitochondrial profiles in painful diabetic neuropathy. Diabetologia. Published 26 January 2026. doi:10.
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