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The molecular mechanism of cardiac aging: the relationship with oxidative stress, telomere length and accumulation of advanced glycation endproducts

Session Cardiac biology and senescence

Speaker Ekaterina Plokhova

Event : ESC Congress 2016

  • Topic : basic science
  • Sub-topic : Basic Science - Cardiac Biology and Physiology
  • Session type : Moderated Posters

Authors : EV Plokhova (Moscow,RU), D Akasheva (Moscow,RU), O Tkacheva (Moscow,RU), I Strazhesko (Moscow,RU), E Dudinskaya (Moscow,RU), V Pykhtina (Moscow,RU), A Kruglikova (Moscow,RU), L Streltsova (Moscow,RU), D Trofimova (Moscow,RU), N Brailova (Moscow,RU), S Boytsov (Moscow,RU)

Authors:
E.V. Plokhova1 , D. Akasheva1 , O. Tkacheva1 , I. Strazhesko1 , E. Dudinskaya1 , V. Pykhtina1 , A. Kruglikova1 , L. Streltsova1 , D. Trofimova1 , N. Brailova1 , S. Boytsov1 , 1National Center of Preventive Medicine - Moscow - Russian Federation ,

Citation:
European Heart Journal ( 2016 ) 37 ( Abstract Supplement ), 423-424

Introduction: Cardiac aging is an independent risk factor for cardiovascular disease (CVD). One of the mechanisms for the cardiac aging can be associated with formation glucose-dependent cross-links of collagen, termed advanced glycation end products (AGEs). AGEs accumulate with age, and can contribute to age-associated changes in the heart such as increased myocardial stiffness and diastolic dysfunction. Methylglyoxal is a byproduct of glucose metabolism and an inducer of AGEs. An excess of methylglyoxal formation can increase free radicals production and cause oxidative stress. Oxidative stressis an important contributor to aging, mainly affecting long-lived postmitotic cells such as cardiac myocytes. These changes lead to accelerated replicative senescence, a marker of which is the length of telomeres. This study examines the role of oxidative stress, telomere shortening and glycation on cardiac aging.

Methods: We investigated 198 non-obese participants aged 60 to 85 years without CVD, diabetes and regular medication. All volunteers underwent standard transthoracic echocardiography using available system (iE33; Philips). Concentration of methylglyoxal in serum was determined using high-performance liquid chromatography with UV detector. Telomere length was measured in eukocyte (LTL) by real-time quantitative polymerase chain reaction. Oxidative stress was determined by assessing the level of malondialdehyde in blood. The association between parameters were evaluated using correlation analysis, logistic regression analysis and analysis of variance (ANOVA) after adjusting for possible confounders.

Results: Short telomeres increases the risk of diastolic dysfunction in the elderly without CVD (χ2=27.78, p=0.001; OR=55.1; 95% CI 12.41–244.87). Older people with shorter telomeres had diastolic dysfunction in 92% of cases. Methylglyoxal was associated with diastolic dysfunction (r=0.23, p=0.015). There was found an association with parameters of pulmonary venous flow. Older subjects with higher methylglyoxal had more impaired left ventricular filling and more pronounced diastolic dysfunction (p<0.01). However methylglyoxal was not related with LTL (p>0.05). We have not received significant association malondialdehyde with methylglyoxal and LTL (p>0.05). Apparently it requires more sensitive markers of oxidative stress.

Conclusions: Our findings suggest that telomere shortening and accumulation AGEs to play an important role in cardiac aging and may be associated with development of age-associated diastolic dysfunction, a significant contributing factor in heart failure in humans. Further research is needed to assess their clinical role in the development of age-related CVD.

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