The TREM2 paradox in fibrosis: a unified mechanism for opposite outcomes across organs
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By
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Xiuping Liang
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Yanhong Li
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Ziyi Tang
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Guan Wang
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Yi Liu
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June 16, 2026
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Clinical Scorecard: The Dual Role of TREM2 in Fibrosis: A Comprehensive Mechanism Explaining Divergent Effects in Different Organs
At a Glance
| Category | Detail |
|---|
| Condition | Organ Fibrosis |
| Key Mechanisms | TREM2 regulates inflammation, repair, and fibrosis through macrophage polarization and immunometabolic reprogramming. |
| Target Population | Patients with chronic diseases leading to organ fibrosis. |
| Care Setting | Clinical settings focusing on chronic inflammatory diseases and fibrosis management. |
Key Highlights
- TREM2 plays a dual role in fibrosis, influencing macrophage behavior.
- In liver fibrosis, TREM2 has antifibrotic effects by enhancing collagen degradation.
- In pulmonary fibrosis, TREM2 expression correlates with fibrosis severity.
- Soluble TREM2 (sTREM2) may serve as a dynamic biomarker.
- TREM2's function varies significantly across different organs.
Guideline-Based Recommendations
Diagnosis
- Assess TREM2 levels as a potential biomarker in fibrotic diseases.
Management
- Consider targeting TREM2 pathways for therapeutic interventions in fibrosis.
Monitoring & Follow-up
- Monitor soluble TREM2 levels to evaluate disease progression.
Risks
- Missense mutations in TREM2 may increase the risk of conditions like Alzheimer's disease.
Patient & Prescribing Data
Individuals with chronic inflammatory conditions leading to organ fibrosis.
Therapeutic strategies may involve modulation of TREM2 signaling pathways.
Clinical Best Practices
- Integrate TREM2 assessment in the evaluation of fibrotic diseases.
- Utilize sTREM2 as a biomarker for monitoring fibrosis progression.
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