ArticleJournal of diabetes research2021
KLF4 Promotes Diabetic Chronic Wound Healing by Suppressing Th17 Cell Differentiation in an MDSC-Dependent Manner.
Article in Journal of diabetes research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Integrative transcriptomic and machine learning analysis identifies candidate biomarkers and immune features in diabetic ulcers.Molecular biology reports · 2026Article
- Zinc-Induced PKCδ-dependent Phosphorylation of MTF-1 Promotes Pulmonary Vascular Remodeling in Hypoxic Pulmonary Hypertension.International journal of biological sciences · 2026Article
- Identifying key targets and immune environment in wound healing based on iron overload-related genes.Archives of dermatological research · 2025Article
- Therapeutic potential of exosomal lncRNAs derived from stem cells in wound healing: focusing on mesenchymal stem cells.Stem cell research & therapy · 2025Review
- Alternative splicing of KLF4 in myeloid cells: implications for cellular plasticity and trained immunity in cancer and inflammatory disease.Frontiers in immunology · 2025Review
- Wound management, healing, and early prosthetic rehabilitation: Part 3 - A scoping review of chemical biomarkers.Canadian prosthetics & orthotics journal · 2025Review
- The reprogramming factor KLF4 in normal and malignant blood cells.Frontiers in immunology · 2025Review
- Identification of Neutrophil Extracellular Trap-Related Biomarkers in Diabetic Foot Ulcers Based on Bioinformatics.Journal of inflammation research · 2025Article
- Histone demethylase JARID1C/KDM5C regulates Th17 cells by increasing IL-6 expression in diabetic plasmacytoid dendritic cells.JCI insight · 2024Article
- IL-17 in wound repair: bridging acute and chronic responses.Cell communication and signaling : CCS · 2024Review
- Hypoxia endothelial cells-derived exosomes facilitate diabetic wound healing through improving endothelial cell function and promoting M2 macrophages polarization.Bioactive materials · 2024Article
- Wound management, healing, and early prosthetic rehabilitation: Part 1 - A scoping review of healing and non-healing definitions.Canadian prosthetics & orthotics journal · 2024Review
- Wound management, healing, and early prosthetic rehabilitation: Part 2 - A scoping review of physical biomarkers.Canadian prosthetics & orthotics journal · 2024Review
- FAM3A reshapes VSMC fate specification in abdominal aortic aneurysm by regulating KLF4 ubiquitination.Nature communications · 2023Article
- The Kruppel-like factor 4-signal transducer and activator of transcription 5A axis promotes pancreatic fibrosis in mice with caerulein-induced chronic pancreatitis.Experimental animals · 2023Article
- Extracellular vesicles from 3D cultured dermal papilla cells improve wound healing via Krüppel-like factor 4/vascular endothelial growth factor A -driven angiogenesis.Burns & trauma · 2023Article
- The role of Th17 cells in endocrine organs: Involvement of the gut, adipose tissue, liver and bone.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesDiabetic wound inflammation deficiencies lead to ulcer development and eventual amputation and disability. Our previous research demonstrates that myeloid-derived suppressor cells (MDSCs) accumulate during inflammation and promote chronic wound healing via the regulation of Kruppel-like factor 4 (KLF4). In this study, we aimed to investigate the potential roles of MDSCs and KLF4 in diabetic wound healing.
methodsAn ob/ob mouse pressure ulcer (PU) model was used to evaluate the process of wound healing. The expression levels of KLF4 and IL-17A were measured by real-time PCR, and the population of MDSCs and Th17 cells was measured by flow cytometry. The levels of cytokines were determined by an immunosuppression assay.
resultsKLF4 deficiency in the diabetic PU model resulted in decreased accumulation of MDSCs, increased expansion of Th17 cells, and significantly delayed wound healing. Conversely, KLF4 activation by APTO-253 accelerated wound healing accompanied by increased MDSC populations and decreased numbers of Th17 cells. MDSCs have been proven to mediate Th17 differentiation via cytokines, and our
conclusionsOur study revealed a previously unreported function of KLF4-regulated MDSCs in diabetic wound healing and identified APTO-253 as a potential agent to improve the healing of pressure ulcers.
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