Karimkhani H. Targeting the CTRP3-PTEN-PI3K/AKT axis in diabetic wound repair: Implications for keratinocyte resilience. World J Diabetes 2026; 17(7): 120721 [DOI: 10.4239/wjd.120721]
Corresponding Author of This Article
Hadi Karimkhani, PhD, Assistant Professor, Medical Biochemistry, Istanbul Okan University, Medical School, Tepeören Mahallesi Tuzla Kampüsü, Istanbul 34959, Türkiye. drhadi.h@gmail.com
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Biochemistry & Molecular Biology
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editorial
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Karimkhani H. Targeting the CTRP3-PTEN-PI3K/AKT axis in diabetic wound repair: Implications for keratinocyte resilience. World J Diabetes 2026; 17(7): 120721 [DOI: 10.4239/wjd.120721]
World J Diabetes. Jul 15, 2026; 17(7): 120721 Published online Jul 15, 2026. doi: 10.4239/wjd.120721
Targeting the CTRP3-PTEN-PI3K/AKT axis in diabetic wound repair: Implications for keratinocyte resilience
Hadi Karimkhani
Hadi Karimkhani, Medical Biochemistry, Istanbul Okan University, Medical School, Istanbul 34959, Türkiye
Author contributions: Karimkhani H was the sole author of this manuscript. The author conceived the editorial concept, performed the literature analysis, drafted the manuscript, revised the manuscript in response to reviewers’ comments, prepared the figure, approved the final version of the manuscript, and agrees to be accountable for all aspects of the work.
AI contribution statement: No AI tool was used for the preparation, drafting, data interpretation, scientific argumentation, conclusion writing, or reference generation of this manuscript. The manuscript was prepared and critically reviewed by the authors. For transparency, the final manuscript was screened using Pangram AI Detector, which classified the document as 100% human-written and 0% AI-generated. In addition, an iThenticate similarity report showed an overall similarity index of 8%, with no integrity flags. These reports can be provided to the editorial office upon request.
Conflict-of-interest statement: The author declares that there are no conflicts of interest related to this manuscript.
Corresponding author: Hadi Karimkhani, PhD, Assistant Professor, Medical Biochemistry, Istanbul Okan University, Medical School, Tepeören Mahallesi Tuzla Kampüsü, Istanbul 34959, Türkiye. drhadi.h@gmail.com
Received: March 10, 2026 Revised: May 10, 2026 Accepted: May 28, 2026 Published online: July 15, 2026 Processing time: 125 Days and 6.4 Hours
Abstract
Diabetes mellitus is associated with impaired wound healing and delayed re-epithelialization, which remain major clinical challenges in diabetic care. Recent findings published in the World Journal of Diabetes by He et al suggest that CTRP3 may contribute to diabetic wound repair by regulating keratinocyte function through the PTEN-PI3K/AKT signaling pathway. Their study showed that CTRP3 expression is reduced under diabetic or high-glucose conditions and increases during normal wound healing. CTRP3 supplementation promoted keratinocyte proliferation, migration, and angiogenic signaling, partly through PTEN suppression and subsequent PI3K/AKT activation. However, the association between CTRP3 and PTEN should be interpreted cautiously, because current evidence does not yet prove a direct, exclusive, or fully validated linear pathway. Further studies using PTEN silencing, PTEN rescue experiments, PI3K/AKT inhibition, time-resolved in vivo wound-tissue validation, and safety-focused human-relevant models will be necessary before CTRP3-based therapeutic strategies can be considered for clinical application.
Core Tip: Diabetic wound healing is severely impaired by metabolic dysregulation, chronic inflammation, and defective keratinocyte function. Emerging evidence highlights CTRP3 as a metabolically responsive adipokine with regenerative potential. Recent experimental findings indicate that CTRP3 promotes keratinocyte proliferation, migration, and angiogenic signaling while suppressing PTEN to activate the PI3K/AKT pathway. This editorial discusses how the CTRP3-PTEN-PI3K/AKT axis integrates metabolic signaling with epithelial repair processes and may represent a promising molecular target for improving diabetic wound healing outcomes.
