Cardiac hypertrophy signaling pathways

Cardiac hypertrophy signaling pathways encompass multiple receptor and intracellular signaling networks activated by mechanical stress, neurohormones (e.g., angiotensin II, endothelin-1, catecholamines), and molecular regulators of cell growth. Key elements include G protein-coupled receptors (α-adrenergic, angiotensin II, endothelin), kinases (PKC, CaMKII, MEK/ERK, PI3K/Akt), effector enzymes (HDACs, p300/CBP), transcription factors (NFAT, MEF2, GATA-4, STAT3), as well as noncoding RNAs. Signaling through these pathways triggers changes in gene expression, protein phosphorylation, chromatin structure, calcium flow, and ultimately drives cardiomyocyte hypertrophy, remodeling, and heart failure if dysregulated. Many of these molecules are recognized as individual therapeutic targets, but "cardiac hypertrophy signaling pathways" as a term refers to the network itself, not a discreet molecular target[1][2][3][4][5][7].

Other names

Signaling pathways mediating cardiac hypertrophyCardiac hypertrophic signalingHypertrophic regulatory pathwaysCardiac remodeling pathways

Inhibit neurohormonal activation (e.g., angiotensin, endothelin, catecholamine signaling); Block Ca2+ influx and downstream calcineurin/NFAT signaling; Modulate kinase activity (e.g., MEK/ERK, PI3K/Akt, PKC, CaMKII); Regulate transcription factors and chromatin remodeling; Target noncoding RNA expression; Enhance angiogenesis via VEGFR-1 stimulation[2]