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. Author manuscript; available in PMC: 2016 Oct 6.
Published in final edited form as: Anal Chem. 2015 Oct 6;87(19):9671–9678. doi: 10.1021/acs.analchem.5b01663

Figure 5.

Figure 5

Schematic of myocardial protein abnormalities in hypertrophic heart. The diagram depicts how mechanical activation of various hypertrophic stimuli via different receptors activates various downstream signaling cascades leading to hypertrophy. Components of the β-adrenergic (β-AR), α-adrenergic (α-AR), and G protein coupled receptor (GPCR) pathways activate protein kinases (PKA, PKG) and MAP kinases. These pathways are involved in inducing fetal proteins (ANP, Tpm2) expression, overexpression, and modification of extracellular matrix proteins (laminin, collagen, fibronectin, LOX), regulatory thin-filament proteins (Acta1, MYLs), and profibrotic pathways which impact myofilament stiffness and contractile function in hypertrophic cardiomyopathy.