Ali J. Marian

This study shows that KDM5A is activated in heart failure and its deletion improves cardiac function and gene expression in a mouse model.

This study shows that KDM5 inhibition promotes iPSC-CM maturation by enhancing fatty acid oxidation, oxidative phosphorylation, and myofibrillar organization through epigenetic regulation of key genes.

The paper identifies a mitofusin 2 mutation (R400Q) that causes mitophagic cardiomyopathy by impairing mitochondrial fusion and Parkin recruitment, distinct from its role in CMT2A.

This study shows that genetic inactivation of beta-catenin improves desmoplakin cardiomyopathy by restoring oxidative phosphorylation gene expression, while its activation worsens the condition.