![]() Cardiac hypertrophy minimizes ventricular wall stress and maintains contractile function when the heart experiences a greater than normal workload ( Grossman et al. The heart adapts to a sustained increase in blood pressure, or a sustained increase in blood volume, by increasing cardiac muscle mass and this growth in myocardium is broadly defined as cardiac hypertrophy ( Linzbach 1976 Bernardo et al. On laisse entendre que le stress oxydatif, les processus inflammatoires, les anomalies de la gestion des ions Ca 2+ dans les cardiomyocytes ainsi que l’apoptose joueraient des rôles critiques dans la dépression de la fonction contractile au cours du développement de l’hypertrophie pathologique. La transition de l’hypertrophie cardiaque physiologique vers l’hypertrophie cardiaque pathologique pourrait être le fait d’une diminution de l’apport sanguin au myocarde hypertrophié comme conséquence de la diminution de la densité des capillaires. C’est pendant l’hypertrophie cardiaque physiologique que le fonctionnement des organites sous-cellulaires, y compris le sarcolemme, le réticulum sarcoplasmique, les mitochondries et les myofibrilles peut être régulé à la hausse, tandis que l’hypertrophie cardiaque pathologique est associée avec une régulation à la baisse de ces activités sous-cellulaires. Aux premiers stades, l’hypertrophie cardiaque est associée avec une fonction cardiaque normale ou améliorée et est considérée comme étant adaptative ou physiologique toutefois, à des stades plus tardifs, si le stimulus n’est pas écarté, elle est associée avec un dysfonctionnement contractile et alors nommée hypertrophie cardiaque pathologique. Ce phénomène permet de réduire au minimum la tension de la paroi ventriculaire dans un cœur soumis à une charge de travail plus élevée que normalement. Le cœur est capable de réagir à des situations de stress par une augmentation de sa masse musculaire, que l’on caractérise plus largement comme étant de l’hypertrophie cardiaque. Oxidative stress, inflammatory processes, Ca 2+-handling abnormalities, and apoptosis in cardiomyocytes are suggested to play a critical role in the depression of contractile function during the development of pathological hypertrophy. The transition of physiological cardiac hypertrophy to pathological cardiac hypertrophy may be due to the reduction in blood supply to hypertrophied myocardium as a consequence of reduced capillary density. It is during physiological cardiac hypertrophy where the function of subcellular organelles, including the sarcolemma, sarcoplasmic reticulum, mitochondria, and myofibrils, may be upregulated, while pathological cardiac hypertrophy is associated with downregulation of these subcellular activities. At initial stages, cardiac hypertrophy is associated with normal or enhanced cardiac function and is considered to be adaptive or physiological however, at later stages, if the stimulus is not removed, it is associated with contractile dysfunction and is termed as pathological cardiac hypertrophy. This phenomenon minimizes ventricular wall stress for the heart undergoing a greater than normal workload. In this Review, we summarize the underlying molecular mechanisms of physiological and pathological hypertrophy, with a particular emphasis on the role of metabolic remodelling in both forms of cardiac hypertrophy, and we discuss how the current knowledge on cardiac hypertrophy can be applied to develop novel therapeutic strategies to prevent or reverse pathological hypertrophy.The heart is capable of responding to stressful situations by increasing muscle mass, which is broadly defined as cardiac hypertrophy. ![]() In the past decade, a growing number of studies have suggested that previously unrecognized mechanisms, including cellular metabolism, proliferation, non-coding RNAs, immune responses, translational regulation, and epigenetic modifications, positively or negatively regulate cardiac hypertrophy. Each form of hypertrophy is regulated by distinct cellular signalling pathways. Hypertrophy initially develops as an adaptive response to physiological and pathological stimuli, but pathological hypertrophy generally progresses to heart failure. There are two types of hypertrophy: physiological and pathological. Therefore, in the adult heart, instead of an increase in cardiomyocyte number, individual cardiomyocytes increase in size, and the heart develops hypertrophy to reduce ventricular wall stress and maintain function and efficiency in response to an increased workload. Cardiomyocytes exit the cell cycle and become terminally differentiated soon after birth. ![]()
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