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Precision Medicine Approaches to Antifibrotic Therapy

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Institute for Neurophysiology, Centre for Physiology and Pathophysiology, Medical Faculty and University Hospital of Cologne, University of Cologne, 50931 Cologne, Germany
Interests: DNA repair; nanobiotechnology; inflammation; immunology
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Special Issue Information

Dear Colleagues,

Recent advances in our understanding of fibrotic diseases have highlighted the need for personalized treatment strategies in antifibrotic therapy. This call for papers seeks contributions exploring precision medicine approaches in the development and application of antifibrotic treatments across various organ systems, including but not limited to the lungs, kidneys, liver, and skin. Key areas of interest include biomarker discovery and validation for disease susceptibility, early diagnosis, prognosis, disease progression, and treatment response prediction. We encourage submissions on the molecular endotyping of fibrotic diseases to guide targeted therapies, in addition to pharmacogenomic approaches to optimize antifibrotic drug selection and dosing. The application of machine learning in diagnosis, prognosis, and treatment decision-making is another crucial area for exploration. We also welcome research on the development of novel antifibrotic compounds tailored to specific disease endotypes. Additionally, we seek papers on the integration of multi-omics data (genomics, proteomics, and metabolomics) to enhance personalized treatment strategies and precision medicine approaches in clinical trial design for antifibrotic therapies. The role of environmental and lifestyle factors in personalizing antifibrotic treatments is another important area of investigation. Lastly, we are interested in studies comparing the effectiveness of precision medicine approaches versus standard care in antifibrotic therapy. We welcome original research articles, systematic reviews, meta-analyses, and perspective pieces that address these topics and contribute to advancing the field of precision medicine in antifibrotic therapy. The goal is to move beyond the current "one-size-fits-all" approach and develop more effective, tailored treatments that can improve outcomes for patients with fibrotic diseases.

Please note that this Special Issue is focused on molecular research; therefore, pure clinical research will not be accepted. However, clinical submissions including biomolecular experiments are welcome for consideration.

Dr. Karim Daliri
Guest Editor

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Keywords

  • fibrotic diseases
  • antifibrotic therapy
  • antifibrotic drug
  • multi-omics data
  • precision medicine

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Published Papers (1 paper)

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Research

13 pages, 1459 KiB  
Article
Modulating Collagen I Expression in Fibroblasts by CRISPR-Cas9 Base Editing of the Collagen 1A1 Promoter
by Karim Daliri, Jürgen Hescheler, Gregory A. Newby, Kendell Clement, David R. Liu and Kurt Pfannkuche
Int. J. Mol. Sci. 2025, 26(7), 3041; https://doi.org/10.3390/ijms26073041 - 26 Mar 2025
Viewed by 452
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 [...] Read more.
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. Full article
(This article belongs to the Special Issue Precision Medicine Approaches to Antifibrotic Therapy)
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