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First-pass extracted concept

extracellular matrix remodeling

Candidate: concept label2 source documents6 linked claims
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Aliases

dysregulated ECM remodeling, ECM remodeling

Extracted Explainers

What the tool is doing

This is the central topic of the review, covering how extracellular matrices are remodeled in development and disease.

Source 2DOIPubMed

What problem it solves

It provides a conceptual frame for linking matrix degradation, crosslinking, and signaling to tissue morphogenesis and pathology.

Source 2DOIPubMed

What it does not solve

The supplied evidence does not support extraction of specific experimental protocols or validated tool performance from this review alone.

Source 2DOIPubMed

Alternatives

Adjacent organizing concepts in the supplied summary include matrisome annotation, protease-centered remodeling, and basement membrane dynamics.

Source 2DOIPubMed

Evidence Snippets

Increasing evidence indicates that dysregulated ECM remodeling is an upstream driver of chronic human diseases rather than a passive consequence of injury.
Evidence 1Source 1DOIPubMedprovenance
The review title is 'Remodelling the extracellular matrix in development and disease'.
Evidence 2Source 2DOIPubMedprovenance

Supporting Sources

Linked Claims

Claim 1mechanistic modelsupports2026Source 1DOIPubMed

Across organs, altered matrix composition, excessive crosslinking, and stiffness-dependent mechanotransduction including integrin-FAK and YAP/TAZ pathways form a self-reinforcing cycle that sustains fibroinflammation, myofibroblast persistence, and progressive tissue dysfunction.

Quoted textsource-backed
Across organs, a self-reinforcing cycle of altered matrix composition, excessive crosslinking, and stiffness-dependent mechanotransduction (including integrin-FAK and YAP/TAZ pathways) sustains fibroinflammation, myofibroblast persistence, and progressive tissue dysfunction.
Claim 2pathogenesis rolesupports2026Source 1DOIPubMed

Dysregulated extracellular matrix remodeling is described as an upstream driver of chronic human diseases rather than a passive consequence of injury.

Quoted textsource-backed
Increasing evidence indicates that dysregulated ECM remodeling is an upstream driver of chronic human diseases rather than a passive consequence of injury.
Claim 3translational strategysupports2026Source 1DOIPubMed

Translational ECM-targeted strategies focus on modulating ECM synthesis and crosslinking, normalizing rather than ablating matrix architecture, and targeting ECM-cell signaling axes in combination with anti-fibrotic, cytotoxic, or immunotherapeutic regimens.

Quoted textsource-backed
Translational strategies increasingly focus on modulating ECM synthesis and crosslinking, normalizing rather than ablating matrix architecture, and targeting ECM-cell signaling axes in combination with anti-fibrotic, cytotoxic, or immunotherapeutic regimens.
Claim 4tumor ecm effectsupports2026Source 1DOIPubMed

In tumors, aligned and crosslinked extracellular matrix promotes invasion, immune evasion, and therapy resistance and shapes perfusion and drug penetration.

Quoted textsource-backed
In tumors, aligned and crosslinked ECM promotes invasion, immune evasion, and therapy resistance while also shaping perfusion and drug penetration.
Claim 5review scopesupports2014Source 2DOIPubMed

This review synthesizes extracellular matrix remodeling across development and disease.

Quoted textsource-backed
Remodelling the extracellular matrix in development and disease
Claim 6topic emphasissupports2014Source 2DOIPubMed

The review explicitly emphasizes matrix metalloproteinases, ADAMTS proteases, lysyl oxidase-mediated crosslinking, collagen/integrin mechanosignaling, discoidin domain receptors, basement membrane dynamics, and growth-factor/proteoglycan regulation.

Quoted textsource-backed
centers ECM remodeling across development and pathology, with explicit emphasis on matrix metalloproteinases (MMPs), ADAMTS proteases, lysyl oxidase-mediated crosslinking, collagen/integrin mechanosignaling, discoidin domain receptors, basement membrane dynamics, and growth-factor/proteoglycan regulation