Cited by 2,265Protease and Inhibitor MechanismsCellular Mechanics and InteractionsTGF-β signaling in diseases

Extracellular Matrix Degradation and Remodeling in Development and Disease

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Lu, P., Takai, K., Weaver, V. M., Werb, Z.·2011·Cold Spring Harbor Perspectives in Biology

Abstract

The extracellular matrix (ECM) serves diverse functions and is a major component of the cellular microenvironment. The ECM is a highly dynamic structure, constantly undergoing a remodeling process where ECM components are deposited, degraded, or otherwise modified. ECM dynamics are indispensible during restructuring of tissue architecture. ECM remodeling is an important mechanism whereby cell differentiation can be regulated, including processes such as the establishment and maintenance of stem cell niches, branching morphogenesis, angiogenesis, bone remodeling, and wound repair. In contrast, abnormal ECM dynamics lead to deregulated cell proliferation and invasion, failure of cell death, and loss of cell differentiation, resulting in congenital defects and pathological processes including tissue fibrosis and cancer. Understanding the mechanisms of ECM remodeling and its regulation, therefore, is essential for developing new therapeutic interventions for diseases and novel strategies for tissue engineering and regenerative medicine.

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Crossref · 10.1101/cshperspect.a005058

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  • Both MMP11 and MMP15 degrade fibronectin and laminin.

    “both MMP11 and MMP15 degrade fibronectin and laminin (30).”

    From Reprogramming of three-dimensional microenvironments for in vitro hair follicle induction (2022) · cites this paper as [30]

    In “Protein Components of the ECM Are Degraded by Proteinases” (page unavailable), the paper says MMP-3 and MMP-10 target fibronectin and laminin. Searches for MMP-11 and MMP-15 found no passage saying either degrades those proteins. Naming different MMPs does not establish that MMP-11 or MMP-15 cannot do so. (LLM, conf=0.78)

    Experimental — accuracy not yet measured
  • Endothelial cell dysfunction strongly affects arterial stiffness through cellular adhesion molecules, matrix metalloproteinases and collagen molecules.

    “EC dysfunction has been shown to strongly affect arterial stiffness via cellular adhesion molecules (CAMs), matrix metalloproteinases (MMPs) and collagen molecules (COLs)67–71.”

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Authors
Lu, P., Takai, K., Weaver, V. M., & Werb, Z.
Affiliations
University of California, San Francisco (US)
Corresponding author
Werb, Z.
Venue
Cold Spring Harbor Perspectives in Biology
Published
2011-09-14
Volume
3
Issue
12
Pages
a005058-a005058
ISSN
1943-0264 (ISSN-L)
OpenAlex
W2006628284
Cited by
2,265
References
127
Citations by year
2026: 104 · 2025: 174 · 2024: 200 · 2023: 192 · 2022: 224 · 2021: 255 · 2020: 234 · 2019: 169 · 2018: 163 · 2017: 168 · 2016: 144 · 2015: 91 · 2014: 66 · 2013: 53 · 2012: 20
Type
posted content
Language
en
Open access
Locations
  • Cold Spring Harbor Perspectives in Biology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • Research Explorer (The University of Manchester) (submittedVersion)
Funders
  • National Institutes of Health
  • National Cancer Institute (R01CA138818, R01CA057621)
  • National Institute of Environmental Health Sciences (U01ES019458)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (R03HD060807)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Protease and Inhibitor Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
Keywords
extracellular matrix, extracellular matrix degradation, extracellular matrix remodeling, histogenesis, stem cell niche, branching morphogenesis, angiogenesis, bone remodeling, wound healing, fibrosis, cancer, cell invasion, cell differentiation, tissue engineering, regenerative medicine
MeSH terms
Animals, Cell Differentiation, Extracellular Matrix, Models, Biological, Neoplasms, Peptide Hydrolases, Stem Cells, Vertebrates, Signal Transduction, Extracellular Matrix Proteins, Body Patterning, Mice

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