The Therapeutic Potential of Novel and Emerging Anti-fibrotic Drugs

Deadline for manuscript submissions: 30 March 2026.

Guest Editors (3)

Jane  Bourke
Prof. Dr. Jane Bourke 
Department of Pharmacology, Biomedicine Discovery Institute, Monash University, Melbourne, 3168, VIC, Australia
Interests: Airway; Bronchodilator; Precision Cut Lung Slice; Asthma; Fibrosis; Silicosis; COPD; Pharmacology
Chrishan S.  Samuel
Prof. Chrishan S. Samuel 
Cardiovascular Disease Program, Monash Biomedicine Discovery Institute and Department of Pharmacology, Monash University, Clayton, VIC, Australia
Interests: Cardiovascular Fibrosis; Kidney Fibrosis; Airway/Lung Fibrosis; Peptide therapeutics; Stem Cells; Epithelial Repair Factors; Animal Models; Myofibroblast Signal Transduction
Robert  Widdop
Prof. Robert Widdop 
Cardiovascular Disease Program, Monash Biomedicine Discovery Institute, and Department of Pharmacology, Monash University, Clayton VIC, Australia
Interests: Renin Angiotensin System; Hypertension; Cardiovascular Disease; Renal Disease;  Fibrotic Biomarkers

Special Issue Information

Fibrosis (organ scarring) results from an aberrant wound-healing response to organ injury, and is a hallmark of organ dysfunction and failure through excessive extracellular matrix (primarily collagen) build-up. Fibrosis-related diseases affecting the heart, kidney, lung and liver contribute to significant morbidity and mortality in developed countries, presenting a major unmet medical challenge.

Current therapies used to treat fibrotic disorders are often indirect and non-specific, and only slow disease progression whilst often provoking several side-effects. The recent identification of novel therapeutic targets, and the development of new treatment strategies based on them, offers the exciting prospect of more efficacious and safer therapies to treat this debilitating disorder.

This Research Topic, entitled “The Therapeutic Potential of Novel and Emerging Anti-fibrotic Drugs”, seeks articles (reviews and original research articles) on various aspects of fibrosis, that focus on emerging and novel treatments. The scope of this call-out can include mechanisms of drug treatments that target aspects of disease pathogenesis including, but not limited to: genetic and environmental factors; cell death; immune cell infiltration and/or inflammation; hypoxia; oxidative stress; organ hypertrophy; the renin-angiotensin-aldosterone system; transforming growth factor-β1 and its down-stream mediators; epithelial- and/or endothelial-to-mesenchymal cell transition; myofibroblast activation and ECM production; and collagen turnover/degradation.

Published Papers (1 Papers)

Open Access

Review

12 January 2026

The Anti-Fibrotic Potential of GLP-1 and GIP Receptor Agonists in Chronic Inflammatory Disorders: Mechanisms and Therapeutic Horizons

Fibrosis, characterised by the excessive deposition of extracellular matrix via activated fibroblasts, is a pathological feature of several chronic inflammatory disorders, which collectively contribute significantly to global morbidity and mortality. Despite this, current anti-fibrotic therapies are of limited efficacy. However, incretin-based therapies, primarily glucagon-like peptide-1 (GLP-1) receptor agonists, are now emerging as candidate drugs for modulating fibrotic signalling pathways. This review synthesises the growing body of preclinical and clinical evidence that incretin receptor agonists exert direct and indirect anti-fibrotic effects. We detail the molecular mechanisms and survey the promising data across hepatic, cardiac, renal, lung, and joint tissues, which underscore the potential for repurposing of this drug class as a therapeutic strategy for fibro-inflammatory conditions.

Simon W.Jones*
Fibrosis
2026,
4
(1), 10001; 
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