Review3 Biotech2025
Targeting diabetic foot ulcer pathophysiology: altered signaling pathways and 3D scaffold as an emerging treatment strategy.
Review in 3 Biotech, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic wound healing, especially in the context of diabetic foot ulcers, remains a major clinical challenge due to the complex interplay of metabolic, vascular, and cellular dysfunctions caused by chronic hyperglycemia. Impaired healing is driven by weakened inflammatory response, decreased blood vessel formation, reduced collagen production, and impaired fibroblast function. Hyperglycemia activates multiple damaging pathways, including the polyol, protein kinase C, hexosamine, and advanced glycation end-product pathways, which collectively induce oxidative stress and chronic inflammation. In addition, diabetic wounds exhibit impaired responses to hypoxia, marked by reduced expression of hypoxia-inducible factors (HIF-1 and HIF-1α), and elevated phenyl pyruvate, which activate macrophage-driven inflammation through CD36-PPT1-NLRP3 axis. Excessive matrix metalloproteinase (MMP) activity and poor collagen deposition disrupt extracellular matrix remodeling, further compromising tissue repair. Key signaling pathways such as PI3K/Akt, MAPK, TGF-β/SMAD, Notch, NfκB, VEGF, Wnt/β-catenin, and Nrf2 are dysregulated in diabetic wounds, undesirably affecting cell survival, inflammation resolution, and angiogenesis. To overcome these challenges, 3D scaffolds have emerged as an innovative therapeutic approach. Mimicking native ECM, it promotes cell adhesion, proliferation, and differentiation, and also enables controlled delivery of bioactive materials like stem cells, antimicrobials, and growth factors. Fabrication uses advanced materials like hydrogels, nanofibers, and smart polymers; these scaffolds are promising in restoring normal healing dynamics. This review explores the pathophysiology, major dysregulated pathways in DFU, and the evolving role of 3D scaffolds in diabetic wound treatment with supportive evidence of preclinical and clinical studies to improve clinical outcomes and patient's quality of life.
Indexed as
Identifiers
What Socratic holds
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.