Advances in Genetic and Epigenetic Gene Therapy for Diabetic Wound Healing

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Genetics".

Deadline for manuscript submissions: 31 March 2026 | Viewed by 390

Special Issue Editor


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Guest Editor
McGowan Institute for Regenerative Medicine, Department of Surgery, University of Pittsburgh, Pittsburgh, PA 15219, USA
Interests: chronic wounds; wound healing; diet; diabetes; obesity; nutrition; genomics; epigenetics

Special Issue Information

Dear Colleagues,

Diabetic ulcers (DUs), complicated by infection/ischemia/high levels of reactive oxygen species, often suffer from poor perfusion, delayed healing and wound recurrence. Gene therapy is emerging as a promising approach for treating DUs by targeting specific genes to promote healing. This involves using genes, proteins, or peptides to stimulate tissue regeneration, improve angiogenesis and reduce inflammation at the wound site. Recently it has been noted that in addition to changes in gene expression, epigenetic changes also play a role in impaired diabetic wound healing, and thus epigenetic gene therapy has emerged as a promising avenue for treating DUs. This collection will focus on potential genetic and epigenetic gene therapy, including genes, proteins, peptides, DNA methylation modifiers, histone modifiers, microRNAs and others to treat and manage DUs.

Dr. Kanhaiya Singh
Guest Editor

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Keywords

  • chronic wounds
  • DFU
  • wound healing
  • diet
  • diabetes
  • obesity
  • nutrition
  • genomics
  • epigenetics
  • DNA methylation
  • histone modifications

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Published Papers (1 paper)

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Research

20 pages, 6840 KB  
Article
Comprehensive Transcriptomic and Proteomic Analysis of Severe Pressure Ulcer Patients Identifies Molecular Signatures Associated with Impaired T Cell Function
by Kanhaiya Singh
Biomolecules 2025, 15(12), 1682; https://doi.org/10.3390/biom15121682 - 2 Dec 2025
Viewed by 283
Abstract
Pressure ulcers (PUs) result from prolonged pressure and shear forces, which cause local skin and soft tissue injury. Elderly patients with pressure injuries face a higher risk of death. Diabetes presents a significant comorbid condition that increases the risk of PU development due [...] Read more.
Pressure ulcers (PUs) result from prolonged pressure and shear forces, which cause local skin and soft tissue injury. Elderly patients with pressure injuries face a higher risk of death. Diabetes presents a significant comorbid condition that increases the risk of PU development due to underlying neuropathy, vasculopathy, and impaired wound healing. Recent molecular biology research on PU subjects has identified inappropriate responses to inflammatory stressors as a significant risk factor. Systemic manifestations, such as an increased abundance of inflammatory cells and alterations in inflammatory mediators, have been linked to PU formation. The present study adopted a bioinformatics, multi-omic data-mining approach to understand cellular and molecular dysregulation and identify biomarkers that may guide the development of more effective screening, diagnostic, and therapeutic strategies in the management of severe PU subjects. At the RNA level, differential gene expression indicated T cell dysfunction and impaired T cell communication in severe PU subjects. Protein-based analysis further validated this finding, as T lymphocyte functional readouts, such as Th1 cell response, memory T cell activation, and Th17 cell differentiation, were predicted to be downregulated. Taken together, our results show that T lymphocyte function and communication remain impaired in severe PU and could guide the development of a therapeutic cell-based treatment for regenerative medicine. Full article
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