Vascular Smooth Muscle Cells Undergo Telomere-Based Senescence in Human Atherosclerosis: Effects of Telomerase and Oxidative Stress

By Charles Matthews, I. Gorenne, Stephen Scott, N. Figg, P. Kirkpatrick, A. Ritchie, M. Goddard, M. Bennett. Circulation Research, 2006

608 citations recorded by the source corpus.

Subfields: Immunology, Physiology

View Paper: https://www.semanticscholar.org/paper/bcf6ce14e80f1a1b83e40eee713a3941ba63893e

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. J. Campisi
2. M. Demaria
3. C. Patil
4. N. Sharpless
5. F. Rodier
6. R. DePinho
7. G. Owens
8. Adam Freund

In Physiology

1. J. Campisi
2. M. Demaria
3. C. Patil
4. F. Rodier
5. P. Desprez
6. Jean-Philippe Coppé
7. N. Sharpless
8. A. Alimonti

Citations in the corpus

• Aging and aging-related diseases: from molecular mechanisms to interventions and treatments (2022, background): “Studies have shown that both p16 and p21 expression and SA-β-gal activity are increased in plaque VSMCs.(257) Telomere shortening, DNA damage, oxidative stress and epigenetic changes can induce VSMC senescence.”
• Vascular smooth muscle cells in atherosclerosis (2016, background): “Secondary necrosis (after apoptosis) releases both IL1α and IL-1β75 Apoptotic VSMCs are normally cleared from the vessel wall in ≈48 hours because VSMCs themselves are efficient at clearing apoptotic VSMCs.76 However, phagocytosis is delayed in the presence of hyperlipidemia, possibly because of the”
• Cellular Senescence: Aging, Cancer, and Injury. (2019, background): “VSMCs and endothelial cells from human atherosclerotic plaques upregulate a number of senescence markers including SA- -gal, p16, and p21 (133, 223, 229, 336).”
• Telomeres and aging. (2008, background): “More recent studies have linked telomere length in smooth muscle cells with senescence and disease severity in patients with atherosclerosis (141, 150).”
• Senescence-Associated Secretory Phenotypes Reveal Cell-Nonautonomous Functions of Oncogenic RAS and the p53 Tumor Suppressor (2008, background): “osteoarthritis and atherosclerosis [28–30].”
• How stem cells age and why this makes us grow old (2007, background): “A mechanistic basis for this association has been supplied by several reports that suggest links between senescence and age-related diseases of the cardiovascular syste”