Extract

Introduction

Advanced age and cardiovascular diseases are related to alterations in cellular metabolism.1,2 The accumulation of fat, a phenomenon observed in ageing, causes a disturbance in glucose and lipid metabolism altering cardiovascular health.3,4

Current therapeutic approaches focus on the treatment of ‘classic’ risk factors such as arterial hypertension, diabetes mellitus, and hyperlipidaemia. It is believed that at least 90% of cardiovascular diseases could be preventable, if the right targets for prevention can be identified.5 Numerous studies are suggesting that it is possible to delay the ageing process by manipulating cellular metabolism and thus reverse or delay age-associated diseases including cardiovascular diseases.2,6,7 Experimental drugs that can interfere with myocardial metabolism have been tested experimentally and in clinical trials.8–10 Most of them aim at switching the energy substrate of the myocardium in oxygen (O2) restricted diseases to optimize O2 consumption at the expense of optimized energy production. Although some of these therapies showed promising results, the side effects of switching energy substrates can be detrimental to the myocardium.9,11,12 Clearly, a better understanding of the metabolic processes and their role and interactions with the development of cardiovascular diseases is needed.

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