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. Author manuscript; available in PMC: 2016 Feb 3.
Published in final edited form as: Cell Metab. 2015 Feb 3;21(2):174–182. doi: 10.1016/j.cmet.2015.01.013

Figure 3.

Figure 3

Myosin heads protrude from the thick filaments (green) to interact with actin containing thin filaments (yellow). Multiple sites throughout the sarcomere and cardiomyocyte are now the targets for new drug development for heart failure (Red stars). 1. Small molecules like omecamtiv are aimed at myosin ATPase activity to increase or decrease contractility. 2. Antisense or RNAi approaches are being tested to silence mutant alleles but not normal alleles. 3. cMyBP-C phosphorylation can be modified through kinase/phosphatases to modulate its “brake effect” on cross-bridge cycling. 4. Calcium handing in the sarcoplasmic reticulum is a target in development. 5. Palmitoyltransferase-1 can be altered using perhexiline to shift metabolic substrate usage from fatty acid oxidation to glycolysis. 6. The regulation of nitric oxide synthase can be used to change cellular redox state and prevent glutathionylation and dysregulation of myofilament proteins.