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Updated: Feb 15, 2026

Isolation, Culture, and Characterization of Primary Dermal Fibroblasts from Human Keloid Tissue
Published on: July 28, 2023
Metabolic reprogramming in keloid fibroblasts: Aerobic glycolysis and a novel therapeutic strategy
Qi Li1, Zelian Qin1, Fangfei Nie1
1Department of Plastic and Reconstructive Surgery, Peking University Third Hospital, Beijing, 100191, China.
Abstract:
Keloids, tumor-like fibroproliferative cutaneous lesions, were reported in metabolic disturbance. However, the metabolic character remains unclear. The purpose of this study is to determine if glycolytic reprogramming is important for the pathogenesis of keloids and to assess the inhibition potential of glycolysis in keloid treatment. An intracellular metabolic profile assay was used to compare metabolic phenotypes between normal skin fibroblasts and keloid fibroblasts (NFs and KFs). Our data indicated that KFs underwent reprogramming of their metabolic phonotype from oxidative phosphorylation to aerobic glycolysis (Warburg effect) with augmented glycolysis and glycolytic capacity. Both gene and protein assays showed that the expression of glycolytic enzymes was upregulated in KFs compared to NFs. Our data showed higher glucose influx and lactate production in KFs compared to NFs. Furthermore, the proliferation of KFs was suppressed in a dose-dependent and time-dependent manner after inhibition of glycolysis with 2-deoxy-glucose (2-DG). Taken together, these findings suggested that keloids underwent a reprogrammed metabolic phenotype of aerobic glycolysis. This was essential for keloid hyperplasia, and glycolytic inhibitors might provide a potential treatment for keloids.
Insights
Keloid fibroblasts exhibit aerobic glycolysis, a metabolic shift crucial for their growth. Inhibiting this process, known as the Warburg effect, shows potential for keloid treatment.
Area of Science:
- Dermatology
- Metabolic research
- Cancer biology (Warburg effect)
Background:
- Keloids are fibroproliferative skin lesions linked to metabolic disturbances.
- The specific metabolic pathways driving keloid pathogenesis are not well understood.
Purpose of the Study:
- To investigate the role of glycolytic reprogramming in keloid development.
- To evaluate glycolysis inhibition as a potential therapeutic strategy for keloids.
Main Methods:
- Compared metabolic profiles of normal skin fibroblasts (NFs) and keloid fibroblasts (KFs) using intracellular metabolic assays.
- Analyzed gene and protein expression of glycolytic enzymes.
- Assessed the impact of 2-deoxy-glucose (2-DG) on KF proliferation.
Main Results:
- Keloid fibroblasts (KFs) display a metabolic shift towards aerobic glycolysis (Warburg effect) compared to NFs.
- KFs show increased glycolysis, glycolytic capacity, glucose uptake, and lactate production.
- Upregulated expression of glycolytic enzymes was observed in KFs.
- Glycolysis inhibition with 2-DG significantly suppressed KF proliferation.
Conclusions:
- Keloids exhibit a reprogrammed metabolic phenotype characterized by aerobic glycolysis.
- This metabolic reprogramming is essential for keloid hyperplasia.
- Targeting glycolysis with inhibitors presents a promising therapeutic avenue for keloid treatment.
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