The ageing cardiovascular system

Bolton, Emily; Rajkumar, Chakravarthi

doi:10.1017/s0959259810000389

Cited by 33 publications

(27 citation statements)

References 76 publications

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“…Epigenetic modifications such as DNA methylation and histone acetylation are described as post-replication changes in chromatin without any alteration in the basal nucleotide code [51]. These mechanisms are essential in controlling gene activation and silencing, and they are connected to various age-related conditions including atherosclerosis [54]. Epigenetic modifications are therefore utilized as biomarkers of cellular senescence in the vascular endothelial.…”

Section: Endothelial Dysfunction and Epigenetic Modificationsmentioning

confidence: 99%

Endothelial Dysfunction in Obesity-Induced Inflammation: Molecular Mechanisms and Clinical Implications

et al. 2020

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Obesity is characterized by the excessive deposition of fat that may interfere with the normal metabolic process of the body. It is a chronic condition associated with various metabolic syndromes, whose prevalence is grossly increasing, and affects both children and adults. Accumulation of excessive macronutrients on the adipose tissues promotes the secretion and release of inflammatory mediators, including interleukin-6 (IL-6), interleukin 1β, tumor necrotic factor-α (TNF-α), leptin, and stimulation of monocyte chemoattractant protein-1 (MCP-1), which subsequently reduce the production of adiponectin thereby initiating a proinflammatory state. During obesity, adipose tissue synthesizes and releases a large number of hormones and cytokines that alter the metabolic processes, with a profound influence on endothelial dysfunction, a situation associated with the formation of atherosclerotic plaque. Endothelial cells respond to inflammation and stimulation of MCP-1, which is described as the activation of adhesion molecules leading to proliferation and transmigration of leukocytes, which facilitates their increase in atherogenic and thromboembolic potentials. Endothelial dysfunction forms the cornerstone of this discussion, as it has been considered as the initiator in the progression of cardiovascular diseases in obesity. Overexpression of proinflammatory cytokines with subsequent reduction of anti-inflammatory markers in obesity, is considered to be the link between obesity-induced inflammation and endothelial dysfunction. Inhibition of inflammatory mechanisms and management and control of obesity can assist in reducing the risks associated with cardiovascular complications.

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Section: Endothelial Dysfunction and Epigenetic Modificationsmentioning

confidence: 99%

Endothelial Dysfunction in Obesity-Induced Inflammation: Molecular Mechanisms and Clinical Implications

et al. 2020

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“…3 Aged vessels show a number of characteristic pathological processes, many of which are also seen in atherosclerosis. 4,5 For example, aged vessels show reduced medial VSMC number, increased collagen deposition, and fracture of the elastin lamellae, which may lead to vessel dilation and increased lumen size.…”

Section: Pathology Of Normal and Premature Vascular Agingmentioning

confidence: 99%

“…Premature or accelerated vascular aging can be promoted by cardiovascular risk factors, 1,2 and cellular senescence is also observed in patients with atherosclerosis. 3 Atherosclerosis is therefore a disease of both organismal aging and cellular senescence par excellence.…”

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confidence: 99%

Aging and Atherosclerosis

Wang

Bennett

2012

Circulation Research

745

323

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Atherosclerosis is classed as a disease of aging, such that increasing age is an independent risk factor for the development of atherosclerosis. Atherosclerosis is also associated with premature biological aging, as atherosclerotic plaques show evidence of cellular senescence characterized by reduced cell proliferation, irreversible growth arrest and apoptosis, elevated DNA damage, epigenetic modifications, and telomere shortening and dysfunction. Not only is cellular senescence associated with atherosclerosis, there is growing evidence that cellular senescence promotes atherosclerosis. This review examines the pathology of normal vascular aging, the evidence for cellular senescence in atherosclerosis, the mechanisms underlying cellular senescence including reactive oxygen species, replication exhaustion and DNA damage, the functional consequences of vascular cell senescence, and the possibility that preventing accelerated cellular senescence is a therapeutic target in atherosclerosis.

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“…Thus, throughout the lifetime, chronic stretching will cause ‘wear and tear’ on normally elastic arteries, leading to vasculature remodelling (medial thickening) and eventual vasculature stiffness (Bolton & Rajkumar, ). Aged vessels have increased collagen and elastin content (Åstrand et al .…”

Section: Introductionmentioning

confidence: 99%

The role of declining adaptive homeostasis in ageing

Pomatto

Davies

2017

The Journal of Physiology

163

108

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Adaptive homeostasis is "the transient expansion or contraction of the homeostatic range for any given physiological parameter in response to exposure to sub-toxic, non-damaging, signalling molecules or events, or the removal or cessation of such molecules or events" (Davies, 2016). Adaptive homeostasis enables biological systems to make continuous short-term adjustments for optimal functioning despite ever-changing internal and external environments. Initiation of adaptation in response to an appropriate signal allows organisms to successfully cope with much greater, normally toxic, stresses. These short-term responses are initiated following effective signals, including hypoxia, cold shock, heat shock, oxidative stress, exercise-induced adaptation, caloric restriction, osmotic stress, mechanical stress, immune response, and even emotional stress. There is now substantial literature detailing a decline in adaptive homeostasis that, unfortunately, appears to manifest with ageing, especially in the last third of the lifespan. In this review, we present the hypothesis that one hallmark of the ageing process is a significant decline in adaptive homeostasis capacity. We discuss the mechanistic importance of diminished capacity for short-term (reversible) adaptive responses (both biochemical and signal transduction/gene expression-based) to changing internal and external conditions, for short-term survival and for lifespan and healthspan. Studies of cultured mammalian cells, worms, flies, rodents, simians, apes, and even humans, all indicate declining adaptive homeostasis as a potential contributor to age-dependent senescence, increased risk of disease, and even mortality. Emerging work points to Nrf2-Keap1 signal transduction pathway inhibitors, including Bach1 and c-Myc, both of whose tissue concentrations increase with age, as possible major causes for age-dependent loss of adaptive homeostasis.

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The ageing cardiovascular system

Cited by 33 publications

References 76 publications

Endothelial Dysfunction in Obesity-Induced Inflammation: Molecular Mechanisms and Clinical Implications

Endothelial Dysfunction in Obesity-Induced Inflammation: Molecular Mechanisms and Clinical Implications

Aging and Atherosclerosis

The role of declining adaptive homeostasis in ageing

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