A Practical Guide to Accelerating Scarring Research and Finding New Treatments

A comprehensive review from Duke-NUS highlights cutting-edge insights into immune cell behavior, paving the way for targeted therapies to treat fibrosis and reduce harmful tissue scarring worldwide.
Research into the causes and potential treatments for excessive tissue scarring, known as fibrosis, is crucial for nearly a billion people worldwide affected by organ damage in the kidneys, lungs, and other tissues. Recent advancements have allowed scientists to pinpoint the specific immune cells responsible for driving these harmful processes. Key to this progress is the development of single-cell isolation technologies, which enable detailed analysis of individual cells within tissues.
A comprehensive review published in Nature Reviews Immunology by a team from Duke-NUS Medical School compiles insights from over 200 studies, creating an accessible "handbook" to accelerate fibrosis research. This resource emphasizes the pivotal role of macrophages—immune cells with dual capabilities: they can either promote healthy tissue repair or contribute to harmful scarring, depending on their state.
Associate Professor Jacques Behmoaras explains that technological advances now allow scientists to identify which macrophages act as 'troublemakers' in fibrosis. These cells, often marked by specific genes such as TREM2, CD9, and SPP1, originate from monocytes recruited to injured tissues and have been linked to increased scarring in organs like the heart, liver, lungs, and kidneys.
The studies reveal complex communication networks between macrophages and fibroblasts—the cells responsible for producing collagen and other tissue components. In fibrosis, SPP1+ macrophages stimulate fibroblasts to produce excessive scar tissue, disrupting the natural balance. Understanding these interactions is crucial for developing targeted therapies.
Potential treatments are emerging from this knowledge, focusing on disrupting the activity of proteins expressed by macrophages, such as SPP1, CCL5, and TREM2, or inhibiting signals from fibroblasts. By targeting these pathways, researchers aim to prevent or reverse harmful scarring.
Professor Enrico Petretto emphasizes that this compiled knowledge aims to serve as a translational guide, helping researchers worldwide to accelerate the development of effective anti-fibrosis therapies. The ultimate goal is to translate these scientific insights into innovative treatments that could significantly improve outcomes for patients affected by fibrotic diseases.
This strategic 'handbook' represents a significant step toward turning groundbreaking cell biology research into tangible medical applications, offering hope for millions suffering from fibrosis-related conditions.
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