Abstract:Background. This work is a review of preclinical and clinical studies of the role of telomeres and telomerase in the development and progression of coronary heart disease (CHD). Materials and methods. A search for full-text publications (articles, reviews, meta-analyses, Cochrane reviews, and clinical cases) in English and Russian was carried out in the databases PubMed, Oxford University Press, Scopus, Web of Science, Springer, and E-library electronic library using keywords and their combinations. The search… Show more
“…With each cell division, the telomere length shortens and this shortening does not occur at a constant rate, but rather, rapidly declines from birth through age 4 ( Rufer et al, 1999 ; Gasmi et al, 2021 ). The normal telomere length of an adult human is approximately 10–15 thousand base pairs (bp), while the protruding part of the G-chain, including 150–200 bp, can bend and form a loop structure (T-loop) ( Zimnitskaya et al, 2022 ), telomeres shorten ~100 bp for each cell division as a result of incomplete replication and exposure to oxidative stress and inflammation ( Wojcicki et al, 2016a ).…”
Background: Several studies have revealed the negative effects of adiposity on telomere length shortening. However, the results of the studies assessing the negative relationship between obesity and leukocyte telomere length (LTL) are not consistent. This systematic review and meta-analysis are aimed to pool the results of articles assessing the relationship between obesity and LTL among children and adolescents.Methods: To retrieve the related studies, four online databases including PubMed, Embase, ProQuest, and Scopus were searched until May 2022. Observational studies evaluating the relationship between obesity and LTL among apparently healthy children and adolescents (aged ≤18 years) were included in the study. We considered the studies that had reported a mean ± standard deviation of LTL. The random-effects model was used to assess the pooled weighted mean difference (WMD) and a 95% confidence interval (CI).Results: The search yielded seven studies from an initial 3,403 records identified. According to the results of seven articles with 4,546 participants, obesity was associated with LTL shortening among children and adolescents (WMD = −0.081; 95% CI: −0.137 to −0.026; p = 0.004; I2 = 99.9%). Also, no publication bias was observed. According to the results of subgrouping, significant results were only attributed to the studies conducted in Europe, with high quality scores, among overweight and obese adolescents, with a baseline LTL lower than 1, and performed in community-based school settings. Also, according to the subgrouping and meta-regression results, the obesity definition criteria and baseline LTL were the possible sources of between-study heterogeneity.Conclusion: We observed shorter LTL among overweight and obese children and adolescents. To obtain more reliable results, further longitudinal prospective studies with large sample sizes and more consistent and accurate definitions of obesity are required.
“…With each cell division, the telomere length shortens and this shortening does not occur at a constant rate, but rather, rapidly declines from birth through age 4 ( Rufer et al, 1999 ; Gasmi et al, 2021 ). The normal telomere length of an adult human is approximately 10–15 thousand base pairs (bp), while the protruding part of the G-chain, including 150–200 bp, can bend and form a loop structure (T-loop) ( Zimnitskaya et al, 2022 ), telomeres shorten ~100 bp for each cell division as a result of incomplete replication and exposure to oxidative stress and inflammation ( Wojcicki et al, 2016a ).…”
Background: Several studies have revealed the negative effects of adiposity on telomere length shortening. However, the results of the studies assessing the negative relationship between obesity and leukocyte telomere length (LTL) are not consistent. This systematic review and meta-analysis are aimed to pool the results of articles assessing the relationship between obesity and LTL among children and adolescents.Methods: To retrieve the related studies, four online databases including PubMed, Embase, ProQuest, and Scopus were searched until May 2022. Observational studies evaluating the relationship between obesity and LTL among apparently healthy children and adolescents (aged ≤18 years) were included in the study. We considered the studies that had reported a mean ± standard deviation of LTL. The random-effects model was used to assess the pooled weighted mean difference (WMD) and a 95% confidence interval (CI).Results: The search yielded seven studies from an initial 3,403 records identified. According to the results of seven articles with 4,546 participants, obesity was associated with LTL shortening among children and adolescents (WMD = −0.081; 95% CI: −0.137 to −0.026; p = 0.004; I2 = 99.9%). Also, no publication bias was observed. According to the results of subgrouping, significant results were only attributed to the studies conducted in Europe, with high quality scores, among overweight and obese adolescents, with a baseline LTL lower than 1, and performed in community-based school settings. Also, according to the subgrouping and meta-regression results, the obesity definition criteria and baseline LTL were the possible sources of between-study heterogeneity.Conclusion: We observed shorter LTL among overweight and obese children and adolescents. To obtain more reliable results, further longitudinal prospective studies with large sample sizes and more consistent and accurate definitions of obesity are required.
“…Contributing to the confusion, many studies analyze aging in cells that are not responsible for the disease [ 138 , 139 ]. Because of sample collection simplicity, circulating leukocytes rather than vascular endothelial cells are commonly analyzed for telomere attrition [ 140 , 141 , 142 , 143 , 144 , 145 , 146 , 147 , 148 , 149 ]. As might be expected, there is a rough correlation in telomere lengths between different tissues since the entire organism is undergoing progressive cell aging over time.…”
Section: Future Approaches To Cardiovascular Disease Interventionmentioning
Despite progress in biomedical technologies, cardiovascular disease remains the main cause of mortality. This is at least in part because current clinical interventions do not adequately take into account aging as a driver and are hence aimed at suboptimal targets. To achieve progress, consideration needs to be given to the role of cell aging in disease pathogenesis. We propose a model unifying the fundamental processes underlying most age-associated cardiovascular pathologies. According to this model, cell aging, leading to cell senescence, is responsible for tissue changes leading to age-related cardiovascular disease. This process, occurring due to telomerase inactivation and telomere attrition, affects all components of the cardiovascular system, including cardiomyocytes, vascular endothelial cells, smooth muscle cells, cardiac fibroblasts, and immune cells. The unified model offers insights into the relationship between upstream risk factors and downstream clinical outcomes and explains why interventions aimed at either of these components have limited success. Potential therapeutic approaches are considered based on this model. Because telomerase activity can prevent and reverse cell senescence, telomerase gene therapy is discussed as a promising intervention. Telomerase gene therapy and similar systems interventions based on the unified model are expected to be transformational in cardiovascular medicine.
“…In recent years, methods of early diagnosis of AMI and comorbid conditions have been improved, which can play an important role in a personalized approach to its therapy and prognosis of outcomes [5]. Of great interest to Russian and foreign researchers is the problem of developing and introducing into real clinical practice new sensitive and specific biochemical and molecular biomarkers of AMI and vascular cognitive disorders associated with AMI [6,7]. The most studied biomarkers of AMI that have found widespread use in clinical practice are cardiac troponins [8,9].…”
This brief review presents Russian and foreign models of acute myocardial infarction (AMI), which are used to gain new knowledge about the pathophysiology of the development of this disease, as well as to search for sensitive and specific biomarkers of AMI and associated pathologies, including vascular cognitive disorders. However, modeling vascular cognitive disorders associated with AMI is a challenging task. Re-searchers need to take into account the additive effect of ischemia of striated muscles (myocardium or skeletal muscles) and central anesthetics during the simulation of AMI in experimental animals.
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