ArticleCardiovascular diabetology2023
CXCL5 suppression recovers neovascularization and accelerates wound healing in diabetes mellitus.
Article in Cardiovascular diabetology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Establishment and translational evaluation of animal models for skin wound healing: a systematic review.Frontiers in physiology · 2026Pooled it
- Targeting angiogenesis in diabetic wound healing: New insight from chemical architecture to functional outcomes.Journal of pharmaceutical analysis · 2026Review
- IL-1β-mediated interaction between Müller cells and microglia through CXCL1/5-CXCR2 aggravates visual dysfunction in experimental glaucoma.Journal of neuroinflammation · 2026Article
- aFGF rescues high glucose-induced senescent fibroblasts and improves diabetic wound healing by regulating SIRT1/STAT3 pathway.Scientific reports · 2026Article
- Apoptotic vesicles from endothelial cells promote endothelial progenitor cell differentiation and angiogenesis via miR-30a-5p mediated activation of the EGFR/PI3K/AKT/VEGF pathway.Stem cell research & therapy · 2026Article
- Danshen/Huanglian-loaded gelatin/Bletilla striata gum dressings accelerate wound healing in anal fistula by promoting angiogenesis through TGF-β/Smad pathway activation.Journal of molecular histology · 2026Article
- Decreased scleral Wnt5aNature communications · 2025Article
- CXCL5 neutralization mitigates cancer cachexia by disrupting CAF-cancer cell crosstalk.Journal of biomedical science · 2025Article
- Immunomodulatory Mechanisms of Chronic Wound Healing: Translational and Clinical Relevance.MedComm · 2025Review
- Deficiency of Aging-Related Gene Chitinase-Like 4 Impairs Olfactory Epithelium Homeostasis.Cell proliferation · 2025Article
- KLF5 enhances CXCL12 transcription in adipose-derived stem cells to promote endothelial progenitor cells neovascularization and accelerate diabetic wound healing.Cellular & molecular biology letters · 2025Article
- Unfolded protein responses: Dynamic machinery in wound healing.Pharmacology & therapeutics · 2025Review
- Genetic risk variants implicate impaired maintenance and repair of periodontal tissues as causal for periodontitis-A synthesis of recent findings.Periodontology 2000 · 2025Review
- Angiogenesis during diabetic wound repair: from mechanism to therapy opportunity.Burns & trauma · 2025Review
- CCL4 contributes to aging related angiogenic insufficiency through activating oxidative stress and endothelial inflammation.Angiogenesis · 2024Article
- Long-Term Administration of Omeprazole-Induced Hypergastrinemia and Changed Glucose Homeostasis and Expression of Metabolism-Related Genes.BioMed research international · 2024Article
- Correction: CXCL5 suppression recovers neovascularization and accelerates wound healing in diabetes mellitus.Cardiovascular diabetology · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHigher chemokine C-X-C motif ligand 5 (CXCL5) level was observed in type 2 diabetes mellitus (DM) patients; however, its role in diabetic vasculopathy was not clarified. This study aimed to explore the impacts and mechanistic insights of CXCL5 in neovasculogenesis and wound healing in DM.
methodsEndothelial progenitor cells (EPCs) and human aortic endothelial cells (HAECs) were used in vitro. Streptozotocin-induced diabetic mice and Lepr
resultsCXCL5 concentrations were increased in plasma and EPCs culture medium from type 2 DM patients. CXCL5 neutralizing antibody upregulated vascular endothelial growth factor (VEGF)/stromal cell-derived factor-1 (SDF-1) and promoted cell function in EPCs from type 2 DM patients and high glucose-treated EPCs from non-DM subjects as well as HAECs. CXCL5 directly up-regulated interleukin (IL)-1β/IL-6/tumor necrosis factor-α and down-regulated VEGF/SDF-1 via ERK/p65 activation through chemokine C-X-C motif receptor 2 (CXCR2). CXCL5 neutralizing antibody recovered the blood flow after hindlimb ischemia, increased circulating EPC number, and enhanced VEGF and SDF-1 expression in ischemic muscle. CXCL5 suppression promoted neovascularization and wound healing in different diabetic animal models. The above observation could also be seen in streptozotocin-induced CXCL5 knockout diabetic mice.
conclusionsCXCL5 suppression could improve neovascularization and wound healing through CXCR2 in DM. CXCL5 may be regarded as a potential therapeutic target for vascular complications of DM.
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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.