ArticleDiabetes2022
Pathogenic Role of Diabetes-Induced Overexpression of Kallistatin in Corneal Wound Healing Deficiency Through Inhibition of Canonical Wnt Signaling.
Article in Diabetes, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Targeting endothelial ERG to mitigate vascular regression in retinopathies.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Exploring the Therapeutic Potential of Salivary Exosomes in Corneal Epithelial Wound Healing.Investigative ophthalmology & visual science · 2025Article
- Examination of an iPSC model of human eye development reveals progressive emergence of critical embryonic cell types.Scientific reports · 2025Article
- Fatty Acid Desaturase 1 Knockdown Promotes Wound Healing and Functional Recovery of the Corneal Epithelium in Diabetes.Investigative ophthalmology & visual science · 2025Article
- Oxygen uptake at the ocular surface in diabetic animals is impaired in response to central corneal injury.Experimental eye research · 2025Article
- Identification of Wnt-5a Receptors Important in Diabetic and Non-Diabetic Corneal Epithelial Wound Healing.Investigative ophthalmology & visual science · 2025Article
- The multifaceted role of kallistatin in human diseases: mechanistic insights and translational potential.Frontiers in cardiovascular medicine · 2025Review
- Progranulin Facilitates Corneal Repair Through Dual Mechanisms of Inflammation Suppression and Regeneration Promotion.Inflammation · 2024Article
- Article
- Endothelial β-catenin upregulation and Y142 phosphorylation drive diabetic angiogenesis via upregulating KDR/HDAC9.Cell communication and signaling : CCS · 2024Article
- Identification and Validation of the Pyroptosis-Related Hub Gene Signature and the Associated Regulation Axis in Diabetic Keratopathy.Journal of diabetes research · 2024Article
- Reversal of dual epigenetic repression of non-canonical Wnt-5a normalises diabetic corneal epithelial wound healing and stem cells.Diabetologia · 2023Article
- Wnt activation as a potential therapeutic approach to treat partial limbal stem cell deficiency.Scientific reports · 2023Article
- A Method for Real-Time Assessment of Mitochondrial Respiration Using Murine Corneal Biopsy.Investigative ophthalmology & visual science · 2023Article
- Lithium chloride promotes diabetic corneal epithelial wound healing by activating the Wnt/β‑catenin signaling pathway.Experimental and therapeutic medicine · 2023Article
- Collagen Crosslinking for Keratoconus: Cellular Signaling Mechanisms.Biomolecules · 2023Article
- Peroxisome proliferator-activated receptor-α (PPARα) regulates wound healing and mitochondrial metabolism in the cornea.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
It was reported previously that circulation levels of kallistatin, an endogenous Wnt signaling inhibitor, are increased in patients with diabetes. The current study was conducted to determine the role of kallistatin in delayed wound healing in diabetic corneas. Immunostaining and Western blot analysis showed kallistatin levels were upregulated in corneas from humans and rodents with diabetes. In murine corneal wound healing models, the canonical Wnt signaling was activated in nondiabetic corneas and suppressed in diabetic corneas, correlating with delayed wound healing. Transgenic expression of kallistatin suppressed the activation of Wnt signaling in the cornea and delayed wound healing. Local inhibition of Wnt signaling in the cornea by kallistatin, an LRP6-blocking antibody, or the soluble VLDL receptor ectodomain (an endogenous Wnt signaling inhibitor) delayed wound healing. In contrast, ablation of the VLDL receptor resulted in overactivation of Wnt/β-catenin signaling and accelerated corneal wound healing. Activation of Wnt signaling in the cornea accelerated wound healing. Activation of Wnt signaling promoted human corneal epithelial cell migration and proliferation, which was attenuated by kallistatin. Our findings suggested that diabetes-induced overexpression of kallistatin contributes to delayed corneal wound healing by inhibiting the canonical Wnt signaling. Thus, kallistatin and Wnt/β-catenin signaling in the cornea could be potential therapeutic targets for diabetic corneal complications.
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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 Socratic graph.