Title of the Article: Telomeres and Atherosclerosis
Authors of the Article: Sajidah Khan, Anil A Chuturgoon, and Datshana P Naidoo.
Year of Publication : 2012.
Journal Publication: Cardiovascular Journal of Africa. Vol 23, No. 10.
Type of Article
This is a review article because it does not report original research. In other words, the article is based on published articles. Generally, the article surveys and summarizes existing literature on the evidence of the topic “telomeres and atherosclerosis” from previously published articles.
Purpose of the Article
The article aims at reviewing the evidence linking telomere biology to atherosclerosis and also discusses the techniques used to preserve telomere length. Additionally, the study aims at studying telomeres to provide a single marker, the combined influence of ageing, environmental risk, and genetics, in predicting risks as well as identifying people who are at risk of developing Coronary Artery Disease (CAD). This is because of the high incidences of type 2 Diabetes and Premature Coronary Artery Disease (CAD) as well as the assumption that these disorders are premature-ageing syndromes in the community.
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Telomerase and how it relates to Cancer
Telomerase is nucleoprotein structure found in the cells of human bodies (at the extreme ends of our chromosomes) that adds repetitive “caps” called “telomeres” to our DNA strands and is related to the aging process as well as cancer. During cell division, telomeres help protect the strands of the DNA from getting shorter. The shortening may continue until it reaches a critical point where the cell no longer divides. This phenomenon results in the numerous changes we see in aging. In other words, telomerase are subject to shortening at every cycle of cell division; this makes the division of the primary cells of humans to stop once a critical minimum telomere length is reached.
Telomeres activity is strongly correlated with increased risk of cancer, especially during aging and during chronic diseases. The cells of cancerous patients divide more often. This results in their telomeres to become very short. Eventually, these cells die if the telomeres become too short. However, the cells can escape death if they manufacture more telomerase enzyme. Many cancers have shortened telomeres. “High telomerase activity has been also been detected in about 90% of human cancer samples” (Khan, Chuturgoon, Naidoo, 2012). The loss of telomere capping function contributes significantly to the cancer initiation process as well as to the induction of chromosome instability.
The relationship between Oxidative Stress-AKT Pathway and Telomerase Shortening
Numerous factors influence telomere length in proliferating cells. One of these factors that have a significant impact on telomere length in proliferating cells is DNA damage owing to oxidative stress triggered by environmental risk factors. Oxidative stress is a pathophysiological mechanism which is associated with ageing as well as age-related disorders. When DNA strands are exposed to oxidative stress, higher levels of stress biomarkers are produced in telomere sequences than in non-telomere sequences. This results in a strong correlation between oxidative stress and telomerase shortening. This is because oxidative stress induces telomere shortening and free radicles mostly target longer telomeres.
Why Type 2 Diabetes is considered as a Premature-Aging Syndrome
Type 2 Diabetes Mellitus is a disorder that makes sugar or glucose levels to rise higher than normal. Both type 2 diabetes and aging share two significant biological processes; glycation and oxidative stress. Hyperglycaemia and insulin resistance, in type 2 diabetes, have additive effects that hasten the atherosclerosis process. Hyperglycaemia results in the activation of numerous molecular pathways that include the increased activity hexosamine pathways and polyol, activation of protein kinase C, and the manufacture of advanced glycation end products (AGEs). Once these interdependent pathways are activated, they induce cellular damage through oxidative stress which ultimately leads to cellular senescence. Since apoptosis and cellular senescence occurs both in smooth muscle cells, vascular endothelial as well as in multiple cell lines, such as endothelial progenitor cells, type 2 diabetes is regarded as a premature-ageing syndrome.
The relationship between Telomere Length and Type 2 Diabetes Severity
To establish if there is a relationship between telomere length and type 2 diabetes severity, the article reviewed previously published articles related to this topic. The studies compared telomere lengths in patients with different severity of type 2 diabetes. The findings from the studies are that there is a gradation in the severity of telomere shortening in the various patients. Telomere lengths in patients with impaired glucose tolerance, diabetes, and a combination of diabetes and atherosclerotic vascular disease were determined and compared. Shortest telomere length was noted in patients with both diabetes and atherosclerotic disease (Khan, Chuturgoon, Naidoo, 2012). Shorter telomere length was recorded in patients with diabetes compared to those with impaired glucose tolerance (Khan, Chuturgoon, Naidoo, 2012). This shows that telomere length becomes shorter as the severity of type 2 diabetes increases.
A drug that Preserves Telomere Length and its Mechanism of Action
There are numerous ways as well as drugs that are used to preserve telomere length. This ways include intense aerobic physical exercises, meditation to relieve stress, healthy diet, and pharmacological agents. One such drug that preserves telomere length is resveratrol. The mechanism of action of this drug is that it activates telomerase by re-pressing silenced telomerase or enhancing low residual telomerase activity to preserve the length of telomerase.
Author’s Major Conclusion
The numerous functions that the study of telomere dynamics serves is the major conclusion of the author. Firstly, the author states that individuals susceptible to CAD can be identified early by measuring the lengths of their telomeres in the early years of their life. Secondly, he states that the measurement of telomere length is likely a better predictor of Coronary Artery Disease (CAD) as compared to the risk markers that are currently available. This is because telomere length uses numerous risk factors to measure cumulative DNA damage whereas the risk markers that are currently available are single, point measurement in time. Thirdly, the author states that longitudinal assessment of telomere length ought to be carried out from time to time since the process of development as well as the progression of atherosclerosis is clinically silent. I think the above conclusion is the major conclusion made by the author becomes it related to the purpose of the article.
My Opinion on the Conclusion Provided by the Authors
The conclusion made by the author makes sense to me. This is because the author summarizes all the threads of the article and relates them to the primary purpose for writing the article. The author briefly outlines all the findings from the study. In my opinion, I think this is article is valid and reliable. This is because the researcher used peer-reviewed articles and cited all the works of other people. The contents of the articles are also well organized.
References
Khan, S., Chuturgoon, A., and Naidoo, Datshana. (2012). Telomeres and Atherosclerosis. Cardiovasc Journal of Africa. Vol. 23. No. 10.
