ArticleCellular and molecular bioengineering2015
Endothelial Cell Senescence Increases Traction Forces due to Age-Associated Changes in the Glycocalyx and SIRT1.
Article in Cellular and molecular bioengineering, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- Article
- Mechanical Signaling: Molecular Mechanisms, Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2025Review
- Article
- Aging and Altered Gravity: A Cellular Perspective.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- Endothelial Dysfunction and Cardiovascular Disease: Hyperbaric Oxygen Therapy as an Emerging Therapeutic Modality?Journal of cardiovascular development and disease · 2024Review
- CRTC1 is a potential target to delay aging-induced cognitive deficit by protecting the integrity of the blood-brain barrier via inhibiting inflammation.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Review
- Cellular senescence and the blood-brain barrier: Implications for aging and age-related diseases.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Organization, dynamics and mechanoregulation of integrin-mediated cell-ECM adhesions.Nature reviews. Molecular cell biology · 2023Review
- Oscillators in the microvasculature: glycocalyx and beyond.American journal of physiology. Cell physiology · 2022Review
- The endothelial glycocalyx in critical illness: A pediatric perspective.Matrix biology plus · 2022Article
- The Endothelial Glycocalyx: A Possible Therapeutic Target in Cardiovascular Disorders.Frontiers in cardiovascular medicine · 2022Review
- The cellular mechanobiology of aging: from biology to mechanics.Annals of the New York Academy of Sciences · 2021Review
- Stiffness and Aging in Cardiovascular Diseases: The Dangerous Relationship between Force and Senescence.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Endothelial cell (EC) aging and senescence are key events in atherogenesis and cardiovascular disease development. Age-associated changes in the local mechanical environment of blood vessels have also been linked to atherosclerosis. However, the extent to which cell senescence affects mechanical forces generated by the cell is unclear. In this study, we sought to determine whether EC senescence increases traction forces through age-associated changes in the glycocalyx and antioxidant regulator deacetylase Sirtuin1 (SIRT1), which is downregulated during aging. Traction forces were higher in cells that had undergone more population doublings and changes in traction force were associated with altered actin localization. Older cells also had increased actin filament thickness. Depletion of heparan sulfate in young ECs elevated traction forces and actin filament thickness, while addition of heparan sulfate to the surface of aged ECs by treatment with angiopoietin-1 had the opposite effect. While inhibition of SIRT1 had no significant effect on traction forces or actin organization for young cells, activation of SIRT1 did reduce traction forces and increase peripheral actin in aged ECs. These results show that EC senescence increases traction forces and alters actin localization through changes to SIRT1 and the glycocalyx.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.