The TREM2 paradox in fibrosis: a unified mechanism for opposite outcomes across organs - Takeaways - MDSpire

The TREM2 paradox in fibrosis: a unified mechanism for opposite outcomes across organs

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TREM2 is a receptor on macrophages that regulates inflammation, tissue repair, and fibrosis through its signaling pathways.
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The dual role of TREM2 in fibrosis varies by organ, influencing macrophage behavior and extracellular matrix remodeling.
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In liver fibrosis, TREM2 has antifibrotic effects by enhancing macrophage collagen-degrading capabilities.
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In pulmonary fibrosis, increased TREM2 expression correlates with fibrosis severity, complicating its functional understanding.
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The review integrates evidence from multiple organs to elucidate TREM2's role in fibrosis and its potential as a biomarker.