Telomere shortening and increased oxidative stress are restricted to venous tissue in patients with varicose veins: A merely local disease?

2014 ◽  
Vol 19 (2) ◽  
pp. 125-130 ◽  
Author(s):  
Daniela Palmieri ◽  
Giuseppe Cafueri ◽  
Francesco Mongelli ◽  
Annalisa Pezzolo ◽  
Vito Pistoia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Varicose Veins ◽  
Telomere Shortening ◽  
Local Disease ◽  
Venous Tissue

scholarly journals Telomere Shortening and Psychiatric Disorders: A Systematic Review

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1423
Author(s):  
Pedro A. Pousa ◽  
Raquel M. Souza ◽  
Paulo Henrique M. Melo ◽  
Bernardo H. M. Correa ◽  
Tamires S. C. Mendonça ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Psychological Distress ◽  
Mental Disorders ◽  
Psychiatric Disorders ◽  
Telomere Length ◽  
Traumatic Stress ◽  
Molecular Mechanisms ◽  
Cochrane Library ◽  
Telomere Shortening ◽  
Anxiety Depression

Telomeres are aging biomarkers, as they shorten while cells undergo mitosis. The aim of this study was to evaluate whether psychiatric disorders marked by psychological distress lead to alterations to telomere length (TL), corroborating the hypothesis that mental disorders might have a deeper impact on our physiology and aging than it was previously thought. A systematic search of the literature using MeSH descriptors of psychological distress (“Traumatic Stress Disorder” or “Anxiety Disorder” or “depression”) and telomere length (“cellular senescence”, “oxidative stress” and “telomere”) was conducted on PubMed, Cochrane Library and ScienceDirect databases. A total of 56 studies (113,699 patients) measured the TL from individuals diagnosed with anxiety, depression and posttraumatic disorders and compared them with those from healthy subjects. Overall, TL negatively associates with distress-related mental disorders. The possible underlying molecular mechanisms that underly psychiatric diseases to telomere shortening include oxidative stress, inflammation and mitochondrial dysfunction linking. It is still unclear whether psychological distress is either a cause or a consequence of telomere shortening.

scholarly journals Oxidative Stress, Telomere Shortening, and Apoptosis Associated to Sarcopenia and Frailty in Patients with Multimorbidity

2020 ◽  
Vol 9 (8) ◽  
pp. 2669 ◽  
Author(s):  
Máximo Bernabeu-Wittel ◽  
Raquel Gómez-Díaz ◽  
Álvaro González-Molina ◽  
Sofía Vidal-Serrano ◽  
Jesús Díez-Manglano ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Telomere Length ◽  
Prospective Observational Study ◽  
Oxygen Species ◽  
Oxidative Stress Markers ◽  
Blood Leukocytes ◽  
Telomere Shortening ◽  
Blood Samples ◽  
Stress Markers ◽  
Total Antioxidant

Background: The presence of oxidative stress, telomere shortening, and apoptosis in polypathological patients (PP) with sarcopenia and frailty remains unknown. Methods: Multicentric prospective observational study in order to assess oxidative stress markers (catalase, glutathione reductase (GR), total antioxidant capacity to reactive oxygen species (TAC-ROS), and superoxide dismutase (SOD)), absolute telomere length (aTL), and apoptosis (DNA fragmentation) in peripheral blood samples of a hospital-based population of PP. Associations of these biomarkers to sarcopenia, frailty, functional status, and 12-month mortality were analyzed. Results: Of the 444 recruited patients, 97 (21.8%), 278 (62.6%), and 80 (18%) were sarcopenic, frail, or both, respectively. Oxidative stress markers (lower TAC-ROS and higher SOD) were significantly enhanced and aTL significantly shortened in patients with sarcopenia, frailty or both syndromes. No evidence of apoptosis was detected in blood leukocytes of any of the patients. Both oxidative stress markers (GR, p = 0.04) and telomere shortening (p = 0.001) were associated to death risk and to less survival days. Conclusions: Oxidative stress markers and telomere length were enhanced and shortened, respectively, in blood samples of polypathological patients with sarcopenia and/or frailty. Both were associated to decreased survival. They could be useful in the clinical practice to assess vulnerable populations with multimorbidity and of potential interest as therapeutic targets.

scholarly journals Obstructive Sleep Apnea as an Acceleration Trigger of Cellular Senescence Processes through Telomere Shortening

2021 ◽  
Vol 22 (22) ◽  
pp. 12536
Author(s):  
Szymon Turkiewicz ◽  
Marta Ditmer ◽  
Marcin Sochal ◽  
Piotr Białasiewicz ◽  
Dominik Strzelecki ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Circadian Clock ◽  
Chronic Inflammation ◽  
Cellular Senescence ◽  
Molecular Mechanisms ◽  
Telomere Shortening ◽  
Age Related ◽  
Obstructive Sleep

Obstructive sleep apnea (OSA) is chronic disorder which is characterized by recurrent pauses of breathing during sleep which leads to hypoxia and its two main pathological sequelae: oxidative stress and chronic inflammation. Both are also associated with cellular senescence. As OSA patients present with higher prevalence of age-related disorders, such as atrial hypertension or diabetes mellitus type 2, a relationship between OSA and accelerated aging is observable. Furthermore, it has been established that these OSA are associated with telomere shortening. This process in OSA is likely caused by increased oxidative DNA damage due to increased reactive oxygen species levels, DNA repair disruptions, hypoxia, chronic inflammation, and circadian clock disturbances. The aim of the review is to summarize study outcomes on changes in leukocyte telomere length (LTL) in OSA patients and describe possible molecular mechanisms which connect cellular senescence and the pathophysiology of OSA. The majority of OSA patients are characterized by LTL attrition due to oxidative stress, hypoxia and inflammation, which make a kind of positive feedback loop, and circadian clock disturbance.

scholarly journals Telomeres and Telomerase in The Aging Heart

2017 ◽  
Vol 9 (3) ◽  
pp. 129
Author(s):  
Anna Meiliana ◽  
Nurrani Mustika Dewi ◽  
Andi Wijaya
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Stem Cell ◽  
Heart Function ◽  
Heart Diseases ◽  
Diastolic Heart Failure ◽  
Peroxisome Proliferator ◽  
Telomere Shortening ◽  
Peroxisome Proliferator Activated Receptor ◽  
Aging Heart

BACKGROUND: Aging per se is a risk factor for reduced cardiac function and heart diseases, even when adjusted for aging-associated cardiovascular risk factors. Accordingly, aging-related biochemical and cell-biological changes lead to pathophysiological conditions, especially reduced heart function and heart disease.CONTENT: Telomere dysfunction induces a profound p53-dependent repression of the master regulators of mitochondrial biogenesis and function, peroxisome proliferator-activated receptor gamma coactivator (PGC)-1a and PGC-1b in the heart, which leads to bioenergetic compromise due to impaired oxidative phosphorylation and ATP generation. This telomere-p53-PGC mitochondrial/metabolic axis integrates many factors linked to heart aging including increased DNA damage, p53 activation, mitochondrial, and metabolic dysfunction and provides a molecular basis of how dysfunctional telomeres can compromise cardiomyocytes and stem cell compartments in the heart to precipitate cardiac aging.SUMMARY: The aging myocardium with telomere shortening and accumulation of senescent cells restricts the tissue regenerative ability, which contributes to systolic or diastolic heart failure. Moreover, patients with ion-channel defects might have genetic imbalance caused by oxidative stress-related accelerated telomere shortening, which may subsequently cause sudden cardiac death. Telomere length can serve as a marker for the biological status of previous cell divisions and DNA damage with inflammation and oxidative stress. It can be integrated into current risk prediction and stratification models for cardiovascular diseases and can be used in precise personalized treatments.KEYWORDS: aging, telomere, telomerase, aging heart, mitochondria, cardiac stem cell

scholarly journals NIR nanoprobe-facilitated cross-referencing manifestation of local disease biology for dynamic therapeutic response assessment

2020 ◽  
Vol 11 (3) ◽  
pp. 803-811 ◽  
Author(s):  
Zhimin Wang ◽  
Xiangzhao Ai ◽  
Zhijun Zhang ◽  
Yong Wang ◽  
Xiangyang Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Therapeutic Response ◽  
Response Assessment ◽  
Local Disease ◽  
Disease Biology

NIR photoacoustic and upconversion luminescent nanoprobe-facilitated cross-referencing manifestation of oxidative stress-induced liver pathophysiology for dynamic therapeutic response assessment.

scholarly journals Ergothioneine Mitigates Telomere Shortening under Oxidative Stress Conditions

2020 ◽  
pp. 1-14
Author(s):  
Priscilla Samuel ◽  
Menelaos Tsapekos ◽  
Nuria de Pedro ◽  
Ann G. Liu ◽  
J. Casey Lippmeier ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Conditions ◽  
Telomere Shortening

scholarly journals Differential Telomere Shortening in Blood versus Arteries in an Animal Model of Type 2 Diabetes

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Samira Tajbakhsh ◽  
Kamelya Aliakbari ◽  
Damian J. Hussey ◽  
Karen M. Lower ◽  
Anthony J. Donato ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Type 2 Diabetes ◽  
Vascular Dysfunction ◽  
Vascular Complications ◽  
Sirtuin 1 ◽  
Telomere Shortening ◽  
Telomere Attrition ◽  
Clinical Complications

Vascular dysfunction is an early feature of diabetic vascular disease, due to increased oxidative stress and reduced nitric oxide (NO) bioavailability. This can lead to endothelial cell senescence and clinical complications such as stroke. Cells can become senescent by shortened telomeres and oxidative stress is known to accelerate telomere attrition. Sirtuin 1 (SIRT1) has been linked to vascular health by upregulating endothelial nitric oxide synthase (eNOS), suppressing oxidative stress, and attenuating telomere shortening. Accelerated leukocyte telomere attrition appears to be a feature of clinical type 2 diabetes (T2D) and therefore the telomere system may be a potential therapeutic target in preventing vascular complications of T2D. However the effect of T2D on vascular telomere length is currently unknown. We hypothesized that T2D gives rise to shortened leukocyte and vascular telomeres alongside reduced vascular SIRT1 expression and increased oxidative stress. Accelerated telomere attrition was observed in circulating leukocytes, but not arteries, in T2D compared to control rats. T2D rats had blunted arterial SIRT1 and eNOS protein expression levels which were associated with reduced antioxidant defense capacity. Our findings suggest that hyperglycemia and a deficit in vascular SIRT1per seare not sufficient to prematurely shorten vascular telomeres.

In vitro effect of calcium dobesilate on oxidative/inflammatory stress in human varicose veins

2011 ◽  
Vol 26 (8) ◽  
pp. 332-337 ◽  
Author(s):  
O Alda ◽  
M S Valero ◽  
D Pereboom ◽  
P Serrano ◽  
J M Azcona ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Varicose Veins ◽  
Protective Action ◽  
Total Antioxidant Status ◽  
Pharmacokinetic Data ◽  
Calcium Dobesilate ◽  
Similar Action ◽  
Inflammatory Stress ◽  
Vitro Effect

Aim To determine whether calcium dobesilate can act in chronic venous insufficiency by similar antioxidant, anti-inflammatory mechanisms as in diabetic retinopathy. Methods Calcium dobesilate was tested in vitro for its protective action against oxidative/inflammatory stress in human varicose veins. Varicose greater saphenous veins were obtained from 14 patients (11 men, 3 women) aged 53–65 years. Oxidative stress was induced exogenously in the vein segments, with the phenazine methosulphate (PMS)/NADH couple. Total antioxidant status (TAS) and malondialdehyde (MDA) contents were used as markers of oxidative stress. Results Calcium dobesilate significantly prevented oxidative disturbances in the micromolar range. PMS/NADH-dependent TAS decrease was fully prevented with IC50 = 11.4 ± 2.3 µmol/L ( n = 6 veins), whereas MDA increase was fully prevented with IC50 = (102 ± −3) µmol/L ( n = 6 veins). Calcium dobesilate acted quali- and quantitatively like rutin, the reference compound. Comparison with pharmacokinetic data suggests that calcium dobesilate can act at therapeutic concentrations. Conclusion Calcium dobesilate protected human varicose veins against oxidative stress in vitro at levels that correspond to therapeutic concentrations. Further studies are required to investigate whether a similar action is found in varicose veins from patients orally treated with calcium dobesilate.

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