Sakthivel Sadayappan

This study investigates the role of fast skeletal myosin binding protein-C in heart failure, finding that its expression exacerbates cardiac dysfunction and that its deletion improves heart function.

The paper identifies RBBP6-mediated degradation of JUNB as a mechanism causing 3D enhancer-promoter disruption and endothelial dysfunction in diabetes.

This study identifies VASH1 and HYAL1 as potential mediators of cardiovascular target organ injury in youth with high blood pressure using multi-omics profiling.

This paper develops a super-resolution reconstruction framework to improve the quantification of complete spatiotemporal myocardial strains in mice using cardiac MRI.

This study shows engineered bacteria can improve survival and cardiac function after myocardial infarction by enhancing gut barrier integrity and reducing inflammation.

This study investigates the molecular mechanisms of HCM caused by the MYBPC3 D389V variant using cardiac organoids and shows hypercontractility and mitochondrial defects that are rescued by a myosin inhibitor.

This paper introduces an in-silico heart phantom to validate cardiac strain imaging algorithms by simulating 4D cardiac motion and testing strain quantification accuracy.

This study investigates the effects of MyBP-C knockout in skeletal muscle, finding altered length-dependent activation and myofilament structure, with implications for MyBP-C-related diseases.

This study decouples structural OFF/ON states from biochemical SRX/DRX states in myosin using X-ray diffraction and ATP assays in porcine myocardium.

This study identifies sMyBP-C's critical role in skeletal muscle development and function using gene-edited mouse models, showing its necessity for prenatal and postnatal muscle growth and structural integrity.

This study shows that sustained MEK1-ERK1/2 activity in skeletal muscle promotes a fast-to-slow fiber-type switch, suggesting potential therapeutic applications for enhancing muscle metabolic effectiveness.

This study shows that lack of KLF2 in myeloid cells accelerates skeletal muscle regeneration by enhancing inflammation and promoting myogenesis.

The paper shows that MYBPC3 mutations disrupt myosin relaxation states, leading to hyper-contractility in HCM, and that targeting myosin can alleviate these effects.