Cardiomyopathies and Related Changes in Contractility of Human Heart Muscle.
Petr G VikhorevNatalia N VikhorevaPublished in: International journal of molecular sciences (2018)
About half of hypertrophic and dilated cardiomyopathies cases have been recognized as genetic diseases with mutations in sarcomeric proteins. The sarcomeric proteins are involved in cardiomyocyte contractility and its regulation, and play a structural role. Mutations in non-sarcomeric proteins may induce changes in cell signaling pathways that modify contractile response of heart muscle. These facts strongly suggest that contractile dysfunction plays a central role in initiation and progression of cardiomyopathies. In fact, abnormalities in contractile mechanics of myofibrils have been discovered. However, it has not been revealed how these mutations increase risk for cardiomyopathy and cause the disease. Much research has been done and still much is being done to understand how the mechanism works. Here, we review the facts of cardiac myofilament contractility in patients with cardiomyopathy and heart failure.
Keyphrases
- heart failure
- smooth muscle
- skeletal muscle
- hypertrophic cardiomyopathy
- left ventricular
- single cell
- atrial fibrillation
- signaling pathway
- oxidative stress
- cardiac resynchronization therapy
- acute heart failure
- genome wide
- cell therapy
- gene expression
- bone marrow
- induced pluripotent stem cells
- cell proliferation
- dna methylation
- endoplasmic reticulum stress