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

Heart Failure And Type 2 Diabetes Mellitus: Neurohumoral, Histological And Molecular Interconnections

“…Other neurohumoral factors implicated in cardiomyocyte growth are catecholamines, angiotensin II and endothelin-1. By stimulating G-protein coupled receptors, they trigger intracellular pathways including MAPK, PKC, and CaMKII signaling that are strongly associated with cardiomyocyte hypertrophy and (if progressed to maladaptation) development of HF [ 51 , 53 ].…”

“…On the contrary, the eccentric hypertrophic phenotype is caused by volume overload and characterized by elongation of cardiomyocytes due to the addition of sarcomeres in series. These changes lead to an increase in LV volume with relatively normal wall thickness [ 53 , 54 ]. However, in both types of cardiac hypertrophy, an increase in cardiomyocyte size takes place.…”

“…Concentric and eccentric types of myocardial hypertrophy can be distinguished not only by morphology features but also by differences in signaling transduction pathways and protein expression [ 55 ]. Various studies discovered that concentric hypertrophy is primarily mediated by MAPKs (ERK 1/2, JNK, p38), PI3K-Akt, calcineurin-CaMKII pathways, tumor necrotic factor (TNF) - α and angiotensin II [ 50 , 53 , 56 ]. In contrast, eccentric hypertrophy is associated only with PI3K-Akt, JNK and p38 pathways [ 50 , 56 ].…”

Calcium Signaling, Calcineurin and NFAT3 Molecular Pathway in Reprogramming of Fetal Gene (BNP) Expression in Cardiac Hypertrophy and Inhibitors of Cardiac Hypertrophy-Review

“…Activated calcineurin dephosphorylates the NFAT in cytosol (Figure -2). Dephosphorylated NFAT enters the nucleus and activates transcription factors and results in cardiac hypertrophy [17,21,[23][24][25] .…”