ArticleDiabetes2021
Dedicator of Cytokinesis 5 Regulates Keratinocyte Function and Promotes Diabetic Wound Healing.
Article in Diabetes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Molecular plasticity of LAMA3 across the disease spectrum: pathogenic mechanisms and clinical translation.Histochemistry and cell biology · 2026Pooled it
- ATF7 drives diabetic wound healing via NOTCH1 repression and N1ICD-dependent macrophage polarization control.JCI insight · 2026Article
- Hsa_circ_0006969 aggravates keratinocytes from high-glucose injury by sponging miR-375 to promote USP10 and SCD expression.Functional & integrative genomics · 2026Article
- Mitochondrial mGPDH Modulates Fibroblast Function in Diabetic Wound Healing via the SIRT1-c-Myc-TGF-β1 Axis.Diabetes · 2026Article
- Multidimensional Regulatory Mechanisms and Targeted Therapeutic Strategies for Inhibited Keratinocyte Proliferation in Diabetic Wounds.Drug design, development and therapy · 2026Review
- YTHDF2 regulates ACSL4-dependent ferroptosis of keratinocytes in diabetic wound healing.Clinical science (London, England : 1979) · 2025Article
- FGFR2 identified as a NETs-associated biomarker and therapeutic target in diabetic foot ulcers.European journal of medical research · 2025Article
- Liraglutide Promotes Diabetic Wound Healing via Myo1c/Dock5.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Mitochondrial glycerol 3-phosphate dehydrogenase deficiency exacerbates lipotoxic cardiomyopathy.iScience · 2024Article
- Dock5 Deficiency Promotes Proteinuric Kidney Diseases via Modulating Podocyte Lipid Metabolism.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Hypothalamic P62 (SQSTM1) regulates energy balance by modulating leptin signaling.Theranostics · 2024Article
- Targeting DNA methylation and demethylation in diabetic foot ulcers.Journal of advanced research · 2023Review
- Human Keratinocyte-Derived Exosomal MALAT1 Promotes Diabetic Wound Healing by Upregulating MFGE8 via microRNA-1914-3p.International journal of nanomedicine · 2023Article
- The role of mesenchymal stem cell-derived EVs in diabetic wound healing.Frontiers in immunology · 2023Review
- The mouse resource at National Resource Center for Mutant Mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2022Review
- Dock5 activation facilitates diabetic wound healing.Metabolism open · 2021Article
- Platelet-Rich Plasma-Derived Exosomal USP15 Promotes Cutaneous Wound Healing via Deubiquitinating EIF4A1.Oxidative medicine and cellular longevity · 2021Article
Corrections and comments
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Authors and funding
20 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cutaneous wound healing is a fundamental biologic and coordinated process, and failure to maintain this process contributes to the dysfunction of tissue homeostasis, increasing the global burden of diabetic foot ulcerations. However, the factors that mediate this process are not fully understood. Here, we identify the pivotal role of dedicator of cytokinesis 5 (Dock5) in keratinocyte functions contributing to the process of skin wound healing. Specifically, Dock5 is highly upregulated during the proliferative phase of wound repair and is predominantly expressed in epidermal keratinocytes. It regulates keratinocyte adhesion, migration, and proliferation and influences the functions of extracellular matrix (ECM) deposition by facilitating the ubiquitination of transcription factor ZEB1 to activate laminin-332/integrin signaling. Genetic ablation of Dock5 in mice leads to attenuated reepithelialization and granulation tissue formation, and Dock5 overexpression-improved skin repair can be abrogated by LAMA3 knockdown. Importantly, Dock5 expression in the skin edge is reduced in patients and animal models of diabetes, further suggesting a direct correlation between its abundance and healing capability. The rescue of Dock5 expression in diabetic mice causes a significant improvement in reepithelialization, collagen deposition, ECM production, and granulation. Our study provides a potential therapeutic target for wound healing impairment during diabetes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.