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Updated: Oct 18, 2025

Unilateral Lung Volume Analysis Using Micro-CT for Enhanced Assessment of Pulmonary Fibrosis in Preclinical Models
Published on: June 20, 2025
Beyond TGFβ1 - novel treatment strategies targeting lung fibrosis
Claudia Sim1, Emma Lamanna1, Frank Cirnigliaro1
1Monash University, Clayton, Melbourne, Australia.
Abstract:
Fibrosis is a key feature of chronic lung diseases and occurs as a consequence of aberrant wound healing. TGFβ1 plays a major role in promoting fibrosis and is the primary target of current treatments that slow, but do not halt or reverse the progression of disease. Accumulating evidence suggests that additional mechanisms, including excessive airway contraction, inflammation and infections including COVID-19, can contribute to fibrosis. This review summarises experimental and clinical studies assessing the potential beneficial effects of novel drugs that possess a unique suite of complementary actions to oppose contraction, inflammation and remodelling, along with evidence that they also limit fibrosis. Translation of these promising findings is critical for the repurposing and development of improved therapeutics for fibrotic lung diseases.
Insights
Fibrosis in chronic lung diseases involves aberrant wound healing. Novel drugs targeting airway contraction and inflammation show promise in limiting fibrosis progression and may offer improved therapeutic options.
Area of Science:
- Pulmonary Medicine
- Fibrotic Lung Disease Research
- Drug Discovery
Background:
- Fibrosis is a hallmark of chronic lung diseases, stemming from abnormal wound healing processes.
- Transforming growth factor-beta 1 (TGFβ1) is a key driver of fibrosis, targeted by current treatments that offer limited efficacy.
- Airway hyperresponsiveness, inflammation, and infections like COVID-19 are increasingly recognized as contributors to fibrotic lung disease.
Purpose of the Study:
- To review experimental and clinical evidence on novel drugs for fibrotic lung diseases.
- To assess drugs with multifaceted actions against contraction, inflammation, and remodeling.
- To evaluate the potential of these drugs to limit fibrosis progression.
Main Methods:
- Systematic review of experimental and clinical studies.
- Analysis of drug mechanisms targeting airway contraction, inflammation, and remodeling.
- Assessment of drug efficacy in preclinical and clinical models of fibrotic lung disease.
Main Results:
- Novel drug candidates demonstrate complementary actions against key fibrotic pathways.
- Evidence suggests these drugs can oppose airway contraction and inflammation.
- These agents show potential in limiting fibrotic remodeling and disease progression.
Conclusions:
- Emerging therapeutics offer a promising avenue for managing fibrotic lung diseases.
- Repurposing and developing these drugs could lead to more effective treatments.
- Targeting multiple fibrotic mechanisms represents a critical step forward in therapy.
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