Therapy for fibrotic diseases: nearing the starting line
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Updated: May 15, 2026

Unilateral Lung Volume Analysis Using Micro-CT for Enhanced Assessment of Pulmonary Fibrosis in Preclinical Models
Published on: June 20, 2025
Scott L Friedman1, Dean Sheppard, Jeremy S Duffield
1Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029, USA. scott.friedman@mssm.edu
Abstract:
Fibrosis, or the accumulation of extracellular matrix molecules that make up scar tissue, is a common feature of chronic tissue injury. Pulmonary fibrosis, renal fibrosis, and hepatic cirrhosis are among the more common fibrotic diseases, which in aggregate represent a huge unmet clinical need. New appreciation of the common features of fibrosis that are conserved among tissues has led to a clearer understanding of how epithelial injury provokes dysregulation of cell differentiation, signaling, and protein secretion. At the same time, discovery of tissue-specific features of fibrogenesis, combined with insights about genetic regulation of fibrosis, has laid the groundwork for biomarker discovery and validation, and the rational identification of mechanism-based antifibrotic drugs. Together, these advances herald an era of sustained focus on translating the biology of fibrosis into meaningful improvements in quality and length of life in patients with chronic fibrosing diseases.
Insights
Fibrosis, characterized by scar tissue accumulation, affects organs like the lungs, kidneys, and liver. Understanding its common and specific mechanisms advances biomarker discovery and antifibrotic drug development for better patient outcomes.
Area of Science:
- Fibrosis research
- Tissue injury and repair
- Extracellular matrix biology
Background:
- Fibrosis, the excessive accumulation of extracellular matrix, is a hallmark of chronic tissue damage.
- Common fibrotic diseases like pulmonary fibrosis, renal fibrosis, and hepatic cirrhosis present significant unmet clinical needs.
- Recent advances highlight conserved fibrotic mechanisms across tissues and tissue-specific fibrogenesis pathways.
Purpose of the Study:
- To elucidate the common and tissue-specific molecular mechanisms underlying fibrogenesis.
- To explore the role of epithelial injury in fibrotic disease progression.
- To establish a foundation for biomarker discovery and the development of targeted antifibrotic therapies.
Main Methods:
- Review of current literature on fibrosis mechanisms.
- Analysis of conserved and divergent pathways in fibrogenesis.
- Integration of genetic regulation insights with clinical observations.
Main Results:
- A clearer understanding of how epithelial injury triggers cellular dysregulation in fibrosis.
- Identification of tissue-specific fibrotic features and their genetic underpinnings.
- Establishment of a framework for biomarker validation and antifibrotic drug discovery.
Conclusions:
- Advances in understanding fibrosis biology pave the way for novel therapeutic strategies.
- Translating fibrotic disease mechanisms into clinical practice can improve patient quality and length of life.
- A sustained focus on fibrosis research is crucial for addressing unmet clinical needs in fibrotic diseases.
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