ArticleCell reports. Medicine2026
Chemomechanical remodeling of glucocorticoid-sensitive fibroblasts for multimodal synergistic therapy of skin fibrosis.
Article in Cell reports. Medicine, 2026. 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.
- Resveratrol Ameliorates Hypertrophic Scar Formation by Regulating ASIC3-Mediated Fibroblast-Macrophage Crosstalk: A Mechanistic Study.Phytotherapy research : PTR · 2026Article
- Soft tissue mechanosensing and remodeling: the core regulatory role of Piezo/TRPV4 ion channels.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Challenges and opportunities in multimodal synergistic therapy for skin fibrosis encompass elucidating the mechanisms of synergistic treatment, optimizing and developing highly coupled combinations, and eliminating therapeutic resistance. This study reveals that the excessively deposited extracellular matrix of hypertrophic scar not only forms a physical barrier for local drug delivery but also generates high mechanical stress, which drives glucocorticoid insensitivity by activating the FAK-AKT-HDAC2 axis in fibroblasts. Both mechanical and biological barriers result in poor outcomes of triamcinolone acetonide therapy for hypertrophic scars. To address this, a chemomechanical antifibrotic approach is engineered by integrating a microneedle-based transdermal delivery platform, immobilized enzymes, and long-acting sustained-release microspheres. This strategy significantly sensitizes scar fibroblasts by disrupting the fibrotic extracellular matrix and the resultant mechanics-induced cellular programs for drug resistance, thus notably reversing the fibrotic characteristics. These findings uncover a mechanism of glucocorticoid resistance and present a multimodal, self-administrable therapy against fibrosis.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.