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Fibroageing: An ageing pathological feature driven by dysregulated extracellular matrix-cell mechanobiology
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Aging causes numerous damages in the long-lived protein components of the extracellular matrix, including advanced glycation end products (AGE), carbonylation and carbamylation, elastin fragmentation, and collagen crosslinking, thus leading to tissue fibrosis (fibroaging).
“Aging causes numerous damages in the long-lived protein components of the extracellular matrix, including advanced glycation end products (AGE), carbonylation and carbamylation, elastin fragmentation, and collagen crosslinking 244 , thus leading to tissue fibrosis (fibroaging) 245 .”
From Hallmarks of aging: An expanding universe (2023) · cites this paper as [245]
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Experimental — accuracy not yet measuredECM 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 [245]
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Cites
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Schafer, M. J., White, T. A., Iijima, K., Haak, A. J., Ligresti, G., Atkinson, E. J., Oberg, A. L., Birch, J., Salmonowicz, H., Zhu, Y., et al. (2017) · Nature Communications · doi:10.1038/ncomms14532 · Cited by 1,613 · cited 1×
“…renal, and lung fibrotic diseases have demonstrated that in ageing, compositional and structural changes in the ECM profoundly influence cell phenotype and function contributing to disease progression throughout several mechanisms (Schafer et al., 2017; Lu et al., 2017; Sturmlechner, 2017).”
BackgroundFibrosis–a common pathway to organ injury and failure
Rockey, D. C., Bell, P. D., & Hill, J. A. (2015) · New England Journal of Medicine · doi:10.1056/nejmra1300575 · Cited by 1,428
Senolytic CAR T cells reverse senescence-associated pathologies
Amor, C., Feucht, J., Leibold, J., Ho, Y.-J., Zhu, C., Alonso-Curbelo, D., Mansilla-Soto, J., Boyer, J. A., Li, X., Giavridis, T., et al. (2020) · Nature · doi:10.1038/s41586-020-2403-9 · Cited by 1,098
PINK1 deficiency impairs mitochondrial homeostasis and promotes lung fibrosis
Bueno, M., Lai, Y.-C., Romero, Y., Brands, J., St. Croix, C. M., Kamga, C., Corey, C., Herazo-Maya, J. D., Sembrat, J., Lee, J. S., et al. (2015) · Journal of Clinical Investigation · doi:10.1172/jci74942 · Cited by 627
Hepatocyte telomere shortening and senescence are general markers of human liver cirrhosis
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NOTCH1 mediates a switch between two distinct secretomes during senescence
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TGF-β Signaling in Cellular Senescence and Aging-Related Pathology
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Stretch-induced Activation of Transforming Growth Factor-β1 in Pulmonary Fibrosis
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Metadata
- Authors
- Selman, M., & Pardo, A.
- Venue
- Ageing Research Reviews
- Publisher
- Elsevier BV
- Published
- 2021-09
- Volume
- 70
- Pages
- 101393
- ISSN
- 1568-1637
- Cited by
- 211
- References
- 13
- Language
- en
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