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Insights & Research

Latest updates on fibrosis research, biomarkers, and drug development trends.

The Roadmap to MASH Complete Remission: Cracking the 'Monotherapy Ceiling' with Combination Therapy

Resmetirom alone: 25% fibrosis improvement. Semaglutide: 37%. The majority DON'T improve. The answer? Combination therapy. We map out the optimal FGF21 + GLP-1 + THR-β combos for the Post-Monotherapy era.

The Semaglutide Reality Check: Can 'Metabolic Fix' Alone Cure Fibrosis?

Semaglutide's ESSENCE trial delivered 63% MASH resolution—but only 37% fibrosis improvement. Is 'Lose weight, cure liver' the whole truth? We explore the limits in Lean MASH and when to use Resmetirom instead.

Post-Rezdiffra MASH Drug Discovery: Target Strategies to Win in the Era After Resmetirom

Resmetirom was approved in 2024—the first MASH drug ever. But with ~25% fibrosis improvement, 75% of patients still need better options. What's the winning Post-Rezdiffra strategy? We decode the science of THR-β and MAESTRO-NASH.

Wnt/β-catenin: Why Does a 'Developmental Pathway' Cause Fibrosis? Bridging Regeneration and Drug Discovery

The developmental program that builds fetal organs, when reactivated in adults, can trigger fibrosis. Why does 'Wnt reactivation' occur in mature tissue? We explore TGF-β crosstalk and the Wnt pathway's potential as a drug target.

The Inflammation-to-Fibrosis Tipping Point: An Immunological Approach to Finding the Drug Window

Chronic inflammation causes fibrosis—that's known. But WHEN is the 'tipping point'? We decode M1→M2 macrophage polarization, TGF-β duality, and EMT to identify the optimal timing for therapeutic intervention.

Mechanisms of Inflammation and Resolution: The Active Process Preventing Chronicity

Inflammation is not just a defense response but a crucial step towards tissue repair. We explain the initiation of acute inflammation, the active "resolution" via SPMs (Specialized Pro-resolving Mediators) and Efferocytosis, and the mechanisms of transition to chronicity.

The Complete Guide to Fibrosis Mechanisms: Myofibroblasts as Drug Targets and Critical Control Points

Why do anti-fibrotic drugs keep failing? The answer lies in controlling the myofibroblast. We systematically explain TGF-β signaling, mechanotransduction, and the 'Achilles heel' for targeted drug discovery.

Myofibroblast Origins and Activation: Why They 'Won't Die'—and How to Find Drug Targets

Myofibroblasts—the executors of fibrosis—should disappear after wound healing. Why do they persist and worsen fibrosis? We explore their origins (resident, pericyte, EMT) and survival signals to identify drug targets.

Anti-fibrotic Drugs List 2026: Approved Therapies & Pipeline Candidates for IPF, MASH and Renal Fibrosis

2026 anti-fibrotic drugs list: approved therapies (Pirfenidone, Nintedanib, Resmetirom) and Phase 2/3 pipeline candidates for IPF, MASH, and renal fibrosis.

Fibrosis Biomarkers (KL-6, SP-D, ELF Score): Diagnosis and Treatment Monitoring

Biomarkers are essential for non-invasive evaluation of fibrosis. We explain the diagnostic value, prognostic ability, and limitations of major markers for lung (KL-6, SP-D), liver (Hyaluronic Acid, ELF Score), heart, and kidney.