Dna Damage, Vascular Senescence, Age Related Atherosclerosis

1715 words - 7 pages


Page 1

Have a minute? Good because that might be all it takes to save your life. There are many biological processes that contribute to aging that includes changes at the cellular level that occurs as we mature. Some are inevitable as we age and there are many others that do not have to be a definitive part of our aging plan. There are wide varieties of conditions such as Atherosclerosis that contributes to excessive inflammatory and fibro-proliferative processes that will affect the arteries. Atherosclerosis kills about a half a million people every year. Yet such deaths can be avoided through developing effective therapies to prevent the transition from largely benign age-related vascular changes to pathological atherosclerotic degeneration. Efficient removal of DNA damage can prevent the initiation and progression of atherosclerosis by avoiding the development of vascular cell senescence and/or apoptosis.

Atherosclerosis is defined as being a degenerative disease of the arteries characterized by patchy thickening of the inner lining of the arterial walls, caused by deposits of fatty material (Collins English Dictionary, 2009). Aging and atherosclerosis have something in common and that is, they share several biochemical pathways and similar vascular alterations. Cellular senescence (process by which cells lose their ability to replicate after a finite number of cell divisions) is linked to the pathogenesis of atherosclerosis. Endothelial cells and vascular smooth muscle cells, both derived from human atherosclerotic plaques, show a lower rate of cell proliferation in vitro and undergo senescence earlier than cells from normal vessels (Maria Andreassi, 2008).

Page 2

Consequently, every single person with atherosclerosis has endothelial

dysfunction. A normal artery wall consists of three layers a thin smooth layer (tunica intima) that lines the inside of the artery that helps blood flow, a muscular elastic layer (tunica media) that helps the pulse circulates blood, and a tough outer layer (tunic adventitia) that protects the artery. Endothelial cells prevent toxic, blood-borne substances from penetrating the smooth muscle of the blood vessel. As we age many atherogenic factors, if left unchecked damages the delicate endothelial cells. Endothelial dysfunction allows lipids and toxins to penetrate the endothelial layer and enter smooth muscle cells. This results in the initiation of an oxidative and inflammatory process that starts the development of plaque deposits. The body tries to prevent the invasion of LDL-C from entering the artery walls by activating Macrophages to consume the LDL-C. The Macrophages become enlarged cholesterol enriched cells called Foam Cells that are embedded in the cell walls. The artery walls become saturated with Foam Cells known as Fatty Streaks in the vessel walls. As the Fatty Streaks grow, the body tries to protect the artery from them by surrounding them in the fibrous...


Phenoptosis concept Essay

1060 words - 5 pages . Patients likely affected by AD show telomeres that are significantly shorter than in apparently normal subjects. An age-related dysfunction of endothelial cells could be, at least in part, an explanation for AD, but “a cell senescence model might explain Alzheimer dementia without primary vascular involvement”. There is an association between Alzheimer disease or ARMD and unhealthy lifestyle, which reduces the number of endothelial progenitor

Biology: Echinacea Extracts can Increase Gene Expression and Protein Expression of apoA-I in Human Intestinal Cells

2060 words - 9 pages appears in high concentration. Besides atherosclerosis, the reactive oxygen species are also found to play a part in human cancer development. The reactive oxygen species causes structural alteration in DNA (Wiseman and Halliwell, 1996), such as base pair mutation, deletion and insertion. It also affects signal transduction pathways in the cytoplasm and the nucleus. For example, H2O2 displaces the inhibitory subunits from nuclear factor kB, a


1150 words - 5 pages found that CVDs are responsible for the deaths of more than 17 million people each year, almost a third of total mortality rates, reported by the World Health Organisation (1, 2). The majority of these deaths were strongly related to Coronary Artery Disease of approximately 7.6 million. However, in the latter 15 years mortality rates in relation to CVD’s have significantly reduced according to age in developed countries. According to the World


2316 words - 10 pages , which increases with arterial stiffening. In subjects with mild atherosclerosis, this velocity is actually lower and is only significantly increased in advanced stages whereby calcification starts to occur14. As a result, although atherosclerosis starts at a young age, its symptoms start becoming observable only in older people, smokers and obese individuals whose lifestyle habits accelerate the process of arterial calcification and with it, the

Aging and Cardiovascular Disease

582 words - 3 pages Aging is the predominant risk factor for cardiovascular diseases (1) and contributes to a significantly more severe outcome in patients with acute myocardial infarction (2). This risk is partly attributable to an age-related decline in the ability of vascular cells to resist stress and effectively remodel the arterial wall. Vascular smooth muscle cells are especially important in this regard. Strategies to prevent the premature senescence

Human Telomerase Reverse Transcriptase

1309 words - 5 pages The naked mole-rate (NMR) is a mammal that can live up to three decades while the common household mouse lives up to 4 years. While NMR have died of natural age related causes, death because of cancer hasn't been observed (Liang, et al., 2010). Human telomerase reverse transcriptase (hTERT) role in tumorigenesis is important in the understanding of how cancer develops and grows. Figuring out how and why the NMR is cancer resistance could model

Atherosclerosis and High Fad Diets

1031 words - 4 pages Atherosclerosis Atherosclerosis, which is a chronic inflammatory disease amongst the arteries of the human body, remains the principal cause of cardiovascular related disease (Gets, 2011). Atherosclerosis results from a complicated relationship between different factors such as lipid metabolism, blood coagulation elements, cytokines, hemodynamic stress, and behavioral risk factors. (Singla et al., 2011) The pathogenesis of atherosclerosis

How Coronary Heart Disease Affects Life

2238 words - 9 pages MI or sudden death before 55 years of age in father) (Matfish & Porth, 2009, pg. 484). Unstable angina (UA)/non-ST-segment elevation myocardial infarction (NSTEMI) is considered to be a clinical syndrome of myocardial ischemia ranging from stable angina to MI (Yehhiazarians, Braunstein, & Askari et al, 2000). UA and NSTEMI differ in whether the ischemia is severe enough to cause sufficient myocardial damage to release detectable quantities of

effects of progeria on immune system

1993 words - 8 pages and ageing. Thus, if hyaluronic acid is faced with abnormalities, the processes of maturation and ageing would be disordered. DNA Damage Response Signaling in HGPS Cells: DNA double strand breaks accumulate in HGPS cells, contributing to cellular senescence. As the growth rate of HGPS slows, the amounts of dysmorphic nuclei and γ-H2AX foci (a marker of DNA DSBs) increase. Histone H2AX is phosphorylated to γ-H2AX in response to DSBs during ATM

Age Related Macular Degeneration

3481 words - 14 pages dysfunction in patients with age-related macular degeneration (AMD): possible relationship between AMD and atherosclerosis." Acta ophthalmologica 90: 695-703. Print. 12. Mathew, Shane. "Age Related Macular Degeneration." Kerala Journal of Ophthamology: n. pag. Web. 13. Moore, Kathryn J., and Ira Tabas. "Macrophages in the Pathogenesis of 16 Atherosclerosis." Cell 145.3 (2011): 341-355. Print. 14. Nicolosi, R. J. "Consumption of 2 and 4 egg

Ductal Carcinoma In Situ

2091 words - 9 pages HIF-1α is seen in a greater frequency in BRCA1 mutation-related invasive breast cancer than in sporadic breast cancer and BRCA1 mutation related invasive breast cancer (Van der Groep et. al 1). Growing levels of HIF-1α are found in solid tumors which may be correlated with increased patient mortality and treatment failure rates. Hypoxia through HIF-mediated adaptation, can lead inhibition of p53 mediated cell death within DNA damage. Non HIF

Similar Essays

Ageing: Major Biological Theories Of Skin Ageing Bachelors Essay

2507 words - 11 pages reductase activity in an advancing age are related with increase in phosphorylation of p53 and p66 this further results in cells senescence, ageing and decrease in bone mass. The important point to understand is that the production of ROS level is not limited to a specific tissue or organ. The oxidative damage is considered as one of the most important caused of Cellular senescence. Senescence is known as the decreased proliferative capacity in the skin

Atherosclerosis Essay

1239 words - 5 pages , atherosclerosis (AS) is the most leading cause of death and morbidity in the Western hemisphere. It often targets the aorta and the coronary and cerebral systems, which in turn makes myocardial infracts (heart attack) and cerebral infracts (stroke) as two of its major consequences. AS is a sickness that progresses slowly; it is known to begin in childhood but complications usually appear only in middle-age when arterial lesions are seen to have clinical

Cardiovascular Disease Essay

1300 words - 5 pages of symptoms that arise until it is to late, CVD’s symptoms can disrupt the regular motions of the heart. However, the results that do arise from these unchangeable factors can bring about a conscious effort to prolong their life by managing the way they live. The severity of an individuals reaction to CVD is mainly attributed to the make up of their DNA. Developing CVD is sometimes unavoidable because an individuals age, gender, and heredity

Anthocyanins Essay

1291 words - 6 pages , protecting against oxidative insults, which helps preserving endothelial cells 19. 3.3 The interaction with DNA A research on the interaction of DNA and anthocyanins was carried out in 19991. It was found that calf thymus DNA and anthocyanidin can form a cyanidin-DNA copigmentation complex, and the formation of this complex prior to exposure to OH can protect both the cyanidin and calf thymus DNA from oxidative damage. In addition