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The DOI matches its Crossref record; 14 of the 14 references it cites were found in a registry or an index.

The ECM path of senescence in aging: components and modifiers

Levi, Naama, Papismadov, Nurit, Solomonov, Inna, Sagi, Irit, Krizhanovsky, Valery·2020·The FEBS Journal
DOI 10.1111/febs.15282
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Abstract

The extracellular matrix (ECM) is a key noncellular component in all organs and tissues. It is composed of a large number of proteins including collagens, glycoproteins (GP), and ECM‐associated proteins, which show diversity of biochemical and biophysical functions. The ECM is dynamic both in normal physiology of tissues and under pathological conditions. One cellular phenomenon associated with changes in both ECM components expression and in ECM remodeling enzymes secretion is cellular senescence. It represents a stable state form of cell cycle arrest induced in proliferating cells by various forms of stress. Short‐term induction of senescence is essential for tumor suppression and tissue repair. However, long‐term presence of senescent cells in tissues may have a detrimental role in promoting tissue damage and aging. Up to date, there is insufficient knowledge about the interplay between the ECM and senescence cells. Since changes in the ECM occur in many physiological and pathological conditions in which senescent cells are present, a better understanding of ECM‐senescence interactions is necessary. Here, we will review the functions of the different ECM components and will discuss the current knowledge about their regulation in senescent cells and their influence on the senescence state.

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  • ECM stiffness affects the function of senescent cells, which in turn secrete matrix metalloproteases that amplify the damage of the extracellular matrix, and proteolytically generate damage-associated molecular patterns to activate pro-senescent, pro-fibrotic and proinflammatory pathways.

    “Extracellular matrix stiffness also affects the function of senescent cells, which in turn secrete matrix metalloproteases that amplify the damage of the extracellular matrix 246 , and proteolytically generate damage-associated molecular patterns to activate pro-senescent, pro-fibrotic and proinflammatory pathways 245 .”

    From Hallmarks of aging: An expanding universe (2023) · cites this paper as [246]

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Metadata

Authors
Levi, N., Papismadov, N., Solomonov, I., Sagi, I., & Krizhanovsky, V.
Affiliations
  • Department of Molecular Cell Biology Weizmann Institute of Science Rehovot Israel
  • Biological Regulation Weizmann Institute of Science Rehovot Israel
ORCID
Krizhanovsky, Valery
Venue
The FEBS Journal
Publisher
Wiley
Published
2020-03-20
Volume
287
Issue
13
Pages
2636-2646
ISSN
  • 1742-464X
  • 1742-4658
DOI
10.1111/febs.15282
Cited by
219
References
14
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
Israel Science Foundation (634‐15, 1800/19)

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