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. Author manuscript; available in PMC: 2017 Dec 1.
Published in final edited form as: J Mol Cell Cardiol. 2016 Oct 11;101:35–43. doi: 10.1016/j.yjmcc.2016.10.004

Figure 2. Cardiac phenotype trends related to the extent of RLC phosphorylation.

Figure 2

Phenotype and lifespan of sedentary and stressed mouse models are shown as a function of RLC phosphorylation. Tracings of heart sections from representative mice are shown above the table. In hearts from normal mice and humans, 40% of RLC (0.4 mol phosphate/ mol RLC) is constitutively phosphorylated. In mice, decreased phosphorylation by phosphorylation site knockin mutant [28], cMLCK gene ablation (KO) [21, 35, 36, 54, 55], or overexpression of myosin phosphatase target subunit (MYPT2) [56], is associated with heart failure, which is exacerbated by cardiovascular stresses such as hypertension [54]. Increased phosphorylation by overexpression of MLCK in the heart attenuates hypertrophic responses to stress [38, 54]. Human hearts in failure have reduced RLC phosphorylation [44-47].