Vascular smooth muscle cell senescence in atherosclerosis

Gorenne, Isabelle; Kavurma, Mary M.; Scott, Stephen; Bennett, Martin R.

doi:10.1016/j.cardiores.2006.06.004

Cited by 170 publications

(113 citation statements)

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“…Vascular smooth muscle cell (VSMC) senescence plays an important role in the pathogenesis of atherosclerosis (Gorenne et al, 2006). In this study, the effect of ginsenoside Rg1 on VSMC senescence was investigated, and the related mechanisms were explored.…”

Section: Ink4amentioning

confidence: 99%

Effects of ginsenoside Rg1 on the senescence of vascular smooth muscle cells

Li¹,

Yan²,

Zhang³

et al. 2016

Genet. Mol. Res.

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ABSTRACT. The development of age-related cardiovascular disease is associated with the senescence of vascular cells. This study aimed to investigate the effect of ginsenoside Rg1 on vascular smooth muscle cell (VSMC) senescence. Primary VSMCs were cultured and divided into control, D-galactose (D-gal), Rg1-L, and Rg1-H groups, which were cultured without and with D-gal, and with low-and highconcentrations of Rg1, respectively. D-gal-induced cellular senescence was identified by b-galactosidase staining, and ultrastructural changes within the cells were observed. The expression of p16, p21, and p53 in the four groups of VSMCs was determined by western blotting, and the cell cycle was investigated by flow cytometry. Compared with the control group, there was an obvious change in the ultrastructure of VSMCs in the D-gal group, and the proportion of b-galactosidasepositive cells was significantly increased (P < 0.05). In addition, p16, p21, and p53 expression was significantly increased (P < 0.05) and the cell cycle was arrested in the G0/G1 phase. Compared with the D-gal group, the percentage of positive cells was significantly reduced (P < 0.05) in the Rg1 groups, the expression of p16, p21, and p53 was significantly reduced (P < 0.05), and the number of cells in the G0/G1 phase decreased (P < 0.05). Ginsenoside Rg1 can inhibit VSMC senescence, and the mechanisms may be related to its partial inhibition of the p16 INK4a /Rb and p53-p21Cip1/Waf1 signaling pathways during the cell cycle.

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Section: Ink4amentioning

confidence: 99%

Effects of ginsenoside Rg1 on the senescence of vascular smooth muscle cells

Li¹,

Yan²,

Zhang³

et al. 2016

Genet. Mol. Res.

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“…Así pues, estos factores son los que están implicados con enfermedades de muy diferente espectro que están relacionadas con los telómeros (48)(49)(50). Entre estas enfermedades están las ligadas al envejecimiento: enfermedades de tipo cardiovascular (infarto de miocardio, enfermedad cerebrovascular, enfermedad arterial periférica) (27,36), cirrosis hepática, hipertensión, aterosclerosis, diabetes, cáncer y enfermedades neurodegenerativas (alzhéimer, párkinson) (14,(51)(52)(53)(54). La longitud de los telómeros predice la mortalidad y las enfermedades relacionadas con el envejecimiento (49).…”

Section: Introductionunclassified

Telómeros Y Calidad De La Dieta: Una Revision Sistematica

Marti¹,

Echeverría

Morell‐Azanza

et al. 2017

Nutr Hosp

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Palabras clave:Telómeros. Dieta mediterránea. Estrés oxidative. ADN. ResumenFundamento: existen pocos estudios que hayan evaluado la relación entre la calidad de la dieta y la integridad telómerica en humanos. Los telómeros son regiones de ADN no codificante que se encuentran en los extremos de los cromosomas, cuya longitud además de indicar la esperanza de vida, indica el estado global de salud. El objetivo de la presente revisión sistemática es recopilar la evidencia existente sobre la relación entre la longitud de los telómeros y la calidad de la dieta para conocer el impacto que algunos nutrientes, alimentos y patrones dietéticos pueden tener sobre la homeostasis telomérica y por lo tanto, sobre la salud en general. Material y métodos: se realizó una revisión bibliográfica en la base de datos PubMed para identificar los artículos publicados (en inglés o español) hasta diciembre de 2016 que cumplían los siguientes criterios: incluían sujetos humanos; eran estudios transversales; estudios de casos y controles; estudios de cohortes prospectivos o estudios de intervención; que evaluaban la relación de los nutrientes, alimentos o patrones dietéticos con la longitud de los telómeros. La estrategia de búsqueda incluía las siguientes palabras clave: nutrients or food OR food groups OR diet OR dietary pattern OR eating pattern OR dietary habits OR diet type AND telomere attrition OR telomere length. En total, se incluyeron 19 estudios transversales, cinco estudios de casos y controles, cinco estudios de cohortes prospectivos y dos estudios de intervención, incluyendo aquellos artículos que se encontraron por listas de referencias de otras publicaciones. Resultados: se encontraron asociaciones positivas entre la longitud de los telómeros y la adherencia a la dieta mediterránea y el consumo de verduras y frutas. Los resultados obtenidos para otros nutrientes, alimentos o patrones dietéticos fueron incoherentes, aunque parece que las carnes procesadas, los cereales, el alcohol y las bebidas endulzadas podrían estar asociados con telómeros más cortos. Conclusiones: la intervención dietética, y en particular la promoción de una dieta de estilo mediterráneo, podría desempeñar un papel en la protección de la integridad telomérica. Key words:Telomere. Mediterranean diet. Oxidative stress. DNA. AbstractBackground: Few studies have evaluated the relationship between diet quality and telomere integrity in humans. Telomeres are regions of non-coding DNA localized at the end of each chromosome whose length, in addition to indicating life expectancy, indicates an overall health status. The objective of this systematic review is to compile the existing evidence on the relationship between telomere length and diet quality to further explore the impact that some nutrients, foods and dietary patterns may have on telomere homeostasis and therefore, in precision nutrition strategies. Material and methods: A bibliographic review was performed in the PubMed database to identify published articles (in English or Spanish) until December 201...

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“…On the contrary, we observed that such exposure enhances the stability of atherosclerotic plaques in ApoE -/-mice, by inhibiting the expression of inflammatory cytokines and stimulating accumulation of collagen within the plaques. Further studies will be required to assess how early modification in the plaques of mice exposed to 137 Cs may alter lesion composition at later time points, with special consideration for smooth muscle cell content (since VSMCs are the main cell type responsible for collagen synthesis in the plaque [8]) and inflammatory mediator expression (including TGFβ which is both anti-inflammatory and a stimulant of collagen production).…”

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confidence: 99%

Chronic internal exposure to low dose 137CS induces positive impact on the stability of atherosclerotic plaques by reducing inflammation in APOE-/- MICE

et al. 2015

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After Chernobyl and Fukushima Daï Chi, two major nuclear accidents, large amounts of radionuclides were released in the environment, mostly caesium 137 ( 137 Cs). Populations living in contaminated territories are chronically exposed to radionuclides by ingestion of contaminated food. However, questions still remain regarding the effects of low dose ionizing radiation exposure on the development and progression of cardiovascular diseases. We therefore investigated the effects of a chronic internal exposure to 137 Cs on atherosclerosis in predisposed ApoE -/-mice. Mice were exposed daily to 0, 4, 20 or 100 kBq/l 137 Cs in drinking water, corresponding to range of concentrations found in contaminated territories, for 6 or 9 months. We evaluated plaque size and phenotype, inflammatory profile, and oxidative stress status in different experimental groups. Results did not show any differences in atherosclerosis progression between mice exposed to 137 Cs and unexposed controls. However, 137 Cs exposed mice developed more stable plaques with decreased macrophage content, associated with reduced aortic expression of pro-inflammatory factors (CRP, TNFα, MCP-1, IFNγ) and adhesion molecules (ICAM-1, VCAM-1 and E-selectin). Lesions of mice exposed to 137 Cs were also characterized by enhanced collagen and smooth muscle cell content, concurrent with reduced matrix metalloproteinase MMP8 and MMP13 expression. These results suggest that low dose chronic exposure of 137 Cs in ApoE -/-mice enhances atherosclerotic lesion stability by inhibiting pro-inflammatory cytokine and MMP production, resulting in collagen-rich plaques with greater smooth muscle cell and less macrophage content.

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Vascular smooth muscle cell senescence in atherosclerosis

Cited by 170 publications

References 104 publications

Effects of ginsenoside Rg1 on the senescence of vascular smooth muscle cells

Effects of ginsenoside Rg1 on the senescence of vascular smooth muscle cells

Telómeros Y Calidad De La Dieta: Una Revision Sistematica

Chronic internal exposure to low dose 137CS induces positive impact on the stability of atherosclerotic plaques by reducing inflammation in APOE-/- MICE

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