ArticleJournal of nanobiotechnology2025
An endoplasmic reticulum stress-responsive nanocomposite hydrogel for diabetic wound healing through a fibroblast-immune cell dual regulation hub.
Article in Journal of nanobiotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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Who cites it
3 citing papers in PubMed.
- Immunomodulatory Effects of Clinically Used Fat Emulsion to Promote Angiogenesis and Osteogenesis for Bone Repair.Materials (Basel, Switzerland) · 2026Article
- Novel AI-Driven Precision Strategies in Diabetic Wound Healing: Immunomodulation and Advances in Smart Composite Nanocarriers.Pharmaceutics · 2026Review
- Construction of Smart Hydrogel-Exosome Drug Delivery Platforms and Their Applications in Skin Rehabilitation.International journal of nanomedicine · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Diabetic wounds exhibit excessive endoplasmic reticulum stress (ERS), which can lead to fibroblast dysfunction, abnormal natural killer (NK) cell activation, and imbalanced macrophage polarization. ERS exerts a bidirectional regulatory effect on wound fibroblasts and immune cells; simply inhibiting ERS impedes wound tissue regeneration. Existing hydrogels cannot precisely regulate ERS and synergistically repair multicell functional defects. Monocyte Chemoattractant Protein-1 (MCP-1), synthesized by fibroblasts in diabetic wounds, is a key molecular regulator of ERS and fibroblast function and a hub for fibroblast-immune cell interactions. This study constructed histidine-chitosan-fibroblast growth factor receptor (FGFR) agonist peptide 1 (FAP1)-pGPU6/GFP/Neo MCP-1-shRNA plasmid (HCFD) nanoparticles. The HCFD nanoparticles were loaded onto 3-carboxyphenylboronic acid (PBA)-modified methyl acrylate gelatin (GelMA) hydrogel (GP), forming the nanocomposite hydrogel Gel-PBA-HCFD (GPHCFD). The GPHCFD nanocomposite hydrogel utilizes FAP1 to target FGFR on wound fibroblasts. Under conditions of excessive ERS, GPHCFD nanocomposite hydrogels were triggered to break boric acid bonds and protonate histidine imidazole, thereby achieving the precise release of the plasmid, which could stably knock out the MCP-1 gene in fibroblasts. Notably, GPHCFD exhibited excellent ERS-responsive functionality, significantly reducing MCP-1 expression and alleviating excessive ERS in fibroblasts under in vitro thapsigargin (Tg)-induced high ERS conditions and high ERS environments in diabetic wounds. GPHCFD improved fibroblast proliferation, migration, and collagen secretion functions. Furthermore, GPHCFD inhibited inflammatory factors of NK cells, including TNF-α and IFN-γ, as well as the aberrant proliferation of CD45
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Registered trials
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