ArticleInternational journal of molecular sciences2025
Modulating Collagen I Expression in Fibroblasts by CRISPR-Cas9 Base Editing of the Collagen 1A1 Promoter.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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
7 citing papers in PubMed.
- Protective Effects of Selected Herbal Additives Against Ochratoxin A-Induced Toxicosis and Oxidative Damage in Rabbits.Antioxidants (Basel, Switzerland) · 2026Article
- Nascent extracellular matrix: the missing piece in hydrogel design.Cell biomaterials · 2026Article
- Modeling CAF-tumor interactions to overcome therapy resistance.Journal of experimental & clinical cancer research : CR · 2026Review
- Protocol for permanent gene repression by CRISPR-adenine base editing of promoter CCAAT motifs.STAR protocols · 2025Article
- Mimicking Gastric Cancer Collagen Reorganization with Decellularized ECM-Based Scaffolds.Biology · 2025Review
- Gut microbiota-derived metabolites in keloid and hypertrophic scarring.Frontiers in microbiology · 2025Review
- The Role of Collagen Genetic Variability in Degenerative Disc Disease and Related Conditions.Current genomics · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Fibrotic diseases, contributing to a significant portion of global mortality, highlight the need for innovative therapies. This study explores a novel approach to disrupt the expression of collagen by using adenine base editing to target Col1a1, a key gene driving both fibrosis and cancer metastasis. Editing Col1a1 in fibroblasts demonstrated 18% editing efficiency. An analysis of a specific clone harboring a CCAAT-to-CCGGA mutation in the Col1a1 promoter revealed reduced collagen production. Notably, when wild-type fibroblasts were cultured on the Col1a1-edited matrix, no compensatory collagen upregulation was detected, suggesting a lack of feedback mechanism in fibroblasts. Furthermore, the matrix derived from edited fibroblasts did not support the growth of MCF-7 cancer cells. These findings suggest that Col1a1 gene editing holds promise as a potential therapeutic strategy for fibrotic diseases. Further investigation is warranted to fully elucidate the implications of these findings for fibrosis and cancer.
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Registered trials
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