Molecular mediators, characterization of signaling pathways with descriptions of cellular distinctions in pathophysiology of cardiac hypertrophy and molecular changes underlying a transition to heart failure

The heart is composed of cardiac myocytes, nonmyocytes, and surrounding extracellular matrix. Cardiac hypertrophy (CH) is molecular, cellular, and interstitial changes that manifest clinically as changes in size, shape, and function of the heart in a response to mechanical and neurohormonal stimuli. CH is recognized as an adaptive process to a variety of physiological and pathological conditions. Although adult-onset hypertrophy can ultimately lead to disease, CH is not necessarily maladaptive and can even be beneficial. It enables myocytes to increase their work output, which improves cardiac pump function. The pathophysiology of CH is complex and multifactorial, as it touches on several cellular and molecular systems. Numerous mediators have been found to be involved in its pathogenesis that includes mitogen-activated protein kinases, protein kinase C, insulin-like growth factor-1, phosphoinositide 3-kinase-Akt/protein kinase B, calcineurin-nuclear factor of activated T cell, and mammalian target of rapamycin. CH is usually considered a poor prognostic sign and is associated with nearly all forms of heart failure. Understanding the molecular background of CH is essential to slow down the destined progression to heart failure. CH has been considered as an important risk factor for cardiac morbidity and mortality whose prevalence has increased during the past few decades. This knowledge will allow the identification of novel molecular targets for pharmacological intervention and will assist the future development of therapeutic strategies for managing cardiovascular disorders. This brief review will give a general overview of basic morphology of heart, various molecular signal transduction pathways, the regulators of CH, and molecular changes underlying a transition to heart failure.