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Pathological hypertrophy heart8/19/2023 ![]() ![]() The top lncRNA candidate was overexpressed in hearts with adeno-associated virus vectors and inhibited with antisense locked nucleic acid-GapmeRs to examine its function. RNA sequencing was applied to hearts from mice after 8 weeks of voluntary exercise-induced physiological hypertrophy and cardiomyogenesis or transverse aortic constriction for 2 or 8 weeks to induce pathological hypertrophy or heart failure. Although long noncoding RNAs (lncRNAs) are important in cardiac development and disease, less is known about their roles in physiological hypertrophy or cardiomyogenesis. The mechanisms underlying these differences remain incompletely understood. The former often precedes cardiomyocyte loss and heart failure the latter paradoxically protects the heart and enhances cardiomyogenesis. Physiology (Bethesda) 2014 29:27–38.The heart grows in response to pathological and physiological stimuli. Mechanisms of exercise-induced cardioprotection. The therapeutic potential of miRNAs regulated in settings of physiological cardiac hypertrophy. Intermittent cardiac overload results in adaptive hypertrophy and provides protection against left ventricular acute pressure overload insult. Moreira-Goncalves D, Henriques-Coelho T, Fonseca H, Ferreira R, Padrao AI, Santa C, Vieira S, Silva AF, Amado F, Leite-Moreira A.A prediction model for left ventricular mass in patients at high cardiovascular risk. Meijs MF, Vergouwe Y, Cramer MJ, Vonken EJ, Velthuis BK, Verton DJ, van der Graaf Y, Visseren FL, Mali WP, Doevendans PA, Bots ML SMART study group. ![]() In conclusion, I am in full agreement with the authors’ statement that we need further research to fully elucidate why some cardiac overloading stimuli are beneficial while others are deleterious. Importantly, the adaptive and ‘physiological’ hypertrophy in both the exercise and simulated exercise groups protected against an acute pressure overload insult. In summary, the authors’ results show that regardless of the nature of the controlled intermittent cardiac overload the heart responds favourably and undergoes adaptive hypertrophy. The latter finding is of particular importance because it can indicate an enhanced capacity to support cardiomyocyte energetic cost without compromising the ATP that is needed to maintain intracellular homeostasis. The exercise and simulated exercise groups had lower body weight, faster cardiac relaxation, cardiomyocyte hypertrophy, and improved mitochondrial complex IV and V activity. Following an 8 week protocol, the authors collected data at rest and during cardiac overload induced by banding of the aorta. To answer their question the authors compared three groups of animals: (1) Sedentary+Placebo, (2) Exercise, and (3) Sedentary+Dobutamine (simulated exercise: similar haemodynamic demand to the exercise group). In this issue of The Journal of Physiology, a group of researchers form Portugal performed a study to address the question of whether submitting the heart to intermittent and tolerable amounts of stress, independent of its nature, could induce a cardiac phenotype that would fit within the ‘physiological’ spectrum (Moreira-Goncalves et al. For example, very high intensity/duration exercise can result in unfavourable cardiac structural and electrical cardiac remodelling. Indeed, even the benefits of exercise can be dose dependent. However, data also implicate duration and intensity of the cardiac overload in determining whether the cardiac hypertrophy that develops is ‘pathological’ or ‘physiological’. 2014).Īlthough both types of cardiac hypertrophy are initiated by an overload to the heart, the distinct differences between the two can be attributed to the type of overloading stimuli. In addition, exercise training has been shown to be the only practical and sustainable countermeasure capable of providing cardioprotection by improving myocardial tolerance to ischaemia–reperfusion injury (e.g. On the other hand, ‘physiological’ cardiac hypertrophy can be provoked by exercise training and can lead to increase cardiac size that is characterized by normal cardiac morphology with a normal and/or enhanced cardiac function (Ooi et al. Two common causes of pathological cardiac hypertrophy are high blood pressure (hypertension) and heart valve stenosis, and this type of hypertrophy is considered to be a major independent risk factor for morbidity and mortality (Meijs et al. ‘Pathological’ cardiac hypertrophy is a condition that is characterized by the thickening of the heart muscle, a decrease in the size of the chambers of the heart, and a reduced capacity of the heart to pump blood to the tissues and organs around the body. ![]()
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