Biological ageing and cardiovascular disease

Samani, Nilesh J.; Harst, Pim van der

doi:10.1136/hrt.2007.136010

Cited by 117 publications

(98 citation statements)

References 37 publications

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“…1,2 Hypertension, one of the main risk factors for a number of cardiovascular diseases, is characterized by an accelerated development of age-related endothelial dilator dysfunction. 3 Therefore, the development of therapeutic strategies directed against age-related endothelial function decline will be an important step toward the prevention and treatment of age-related vascular diseases, such as hypertension and coronary artery disease.…”

mentioning

confidence: 99%

Bradykinin Protects Against Oxidative Stress–Induced Endothelial Cell Senescence

Oeseburg¹,

Iusuf²,

Harst³

et al. 2009

Hypertension

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Abstract-Premature aging (senescence) of endothelial cells might play an important role in the development and progression of hypertension and atherosclerosis. We hypothesized that bradykinin, a hormone that mediates vasoprotective effects of angiotensin-converting enzyme inhibitors, protects endothelial cells from oxidative stressinduced senescence. Bradykinin treatment (0.001 to 1 nmol/L) dose-dependently decreased senescence induced by 25 mol/L of H 2 O 2 in cultured bovine aortic endothelial cells, as witnessed by a complete inhibition of increased senescent cell numbers and a 34% reduction of the levels of the senescence-associated cell cycle protein p21. Because H 2 O 2 induces senescence through superoxide-induced DNA damage, single-cell DNA damage was measured by comet assay. Bradykinin reduced DNA damage to control levels. The protective effect of bradykinin also resulted in a significant increase in the migration of H 2 O 2 -treated bovine aorta endothelial cells in an in vitro endothelial injury model, or "scratch" assay. The protective effect of bradykinin was abolished by the bradykinin B2 receptor antagonist HOE-140 and the NO production inhibitor N -methyl-L-arginine acetate salt. Therefore, we conclude that bradykinin protects endothelial cells from superoxide-induced senescence through bradykinin B2 receptor-and NO-mediated inhibition of DNA damage. Key Words: senescence Ⅲ endothelial Ⅲ bradykinin Ⅲ reactive oxygen species Ⅲ DNA damage A ging-related vascular dysfunction is believed to be an important contributor to vascular pathogenesis and a worsened prognosis. 1,2 Hypertension, one of the main risk factors for a number of cardiovascular diseases, is characterized by an accelerated development of age-related endothelial dilator dysfunction. 3 Therefore, the development of therapeutic strategies directed against age-related endothelial function decline will be an important step toward the prevention and treatment of age-related vascular diseases, such as hypertension and coronary artery disease.Endothelial cell senescence is a cyclin-dependent kinase inhibitor 1A (p21) proliferative arrest 4 that can be induced by DNA damage caused by exposure to reactive oxygen species (ROS). 5 There are several reasons to assume that endothelial cell senescence is involved in vascular pathogenesis. Senescent endothelial cells show deleterious functional changes (eg, decreased release of endothelial-derived relaxing factors, increased release of endothelial-derived constricting factors, and increased production of molecules that are associated with inflammation). 6,7 These features are reminiscent of the aberrant endothelial changes observed in aging and atherosclerosis. 8 Moreover, an increase of senescent endothelial cells and senescence markers is observed in the vasculature of atherosclerotic patients and in aged rodents with endothelial dysfunction. 8,9 Angiotensin-converting enzyme (ACE) inhibitors effectively protect against the progression of chronic atherosclerotic disease, endothelial dysfunction, an...

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mentioning

confidence: 99%

Bradykinin Protects Against Oxidative Stress–Induced Endothelial Cell Senescence

Oeseburg¹,

Iusuf²,

Harst³

et al. 2009

Hypertension

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“…Several candidate mechanisms link age to vascular disease, and the telomere hypothesis is the best known of these [47]. Telomeres are DNA-protein complexes located at the end of chromosomes that serve as protective caps and shorten with each cell cycle.…”

Section: As Old As Your Arteriesmentioning

confidence: 99%

How to survive diabetes

Gale

2009

Diabetologia

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“…31 Other studies also found no correlation between telomere length and frailty index. 32,33 Associations between depression and telomere length While many age-related diseases such as cardiovascular disease, 14 type 2 diabetes, 15 neurological disease, 16 and cancer 17 have been associated with a shorter telomere length, an emerging literature implicates depression, highly prevalent in older adults, as a potential pathway toward accelerated aging. Prior work has identified relations of depression to age-related diseases such as diabetes, 34 metabolic disorders, 35 coronary heart disease, 36 cognitive impairments/dementia, 37 and cancer.…”

Section: Telomerase Activity Telomere Length and Agingmentioning

confidence: 99%

Exploring the link between depression and accelerated cellular aging: telomeres hold the key

Yu¹,

Woo²

2015

RRBC

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Accumulating evidence suggests that telomeres may be a marker for biological aging and telomere length may be affected by multifactorial influences, including cumulative exposure to depression. Associations with telomere length have been reported for major depressive disorder, lifetime duration of depression, higher depression severity, and history of depression. The exact underling mechanisms for these associations have yet to be fully elucidated; however, oxidative stress, chronic inflammation, dysregulated hypothalamus-pituitary-adrenal axis, and altered cortisol levels may be important biochemical mediators. These mediators could also be influenced by psychological stress, unhealthy lifestyle behaviors, or other potential factors, such as childhood abuse, post-traumatic stress disorder, and anxiety that are commonly associated with depression. As such, stress reduction and lifestyle interventions that may affect the telomere maintenance system should be considered for individuals with depression.

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Biological ageing and cardiovascular disease

Cited by 117 publications

References 37 publications

Bradykinin Protects Against Oxidative Stress–Induced Endothelial Cell Senescence

Bradykinin Protects Against Oxidative Stress–Induced Endothelial Cell Senescence

How to survive diabetes

Exploring the link between depression and accelerated cellular aging: telomeres hold the key

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