Welcome to the Tampakakis Lab
How does the heart grow and mature?
The transition from fetal to postnatal life marks a profound transformation in cardiac structure, metabolism, and function. During fetal development, cardiomyocytes retain substantial proliferative capacity, exhibit relatively immature contractile organization, and rely predominantly on glycolytic metabolism. Following birth, these cells undergo coordinated structural and metabolic remodeling, characterized by cell-cycle withdrawal, sarcomere maturation, mitochondrial biogenesis, and a shift toward oxidative phosphorylation. These developmental adaptations are essential for establishing the energetic and contractile demands of the mature heart. However, the molecular mechanisms that orchestrate this transition remain incompletely understood, and their dysregulation can contribute to congenital heart disease, cardiomyopathy, and heart failure.
What controls this transformation?
Cardiomyocyte maturation is regulated by complex interactions between genetic, epigenetic, and environmental signals. Our laboratory investigates three interconnected regulatory mechanisms: m6A RNA methylation, sympathetic neuron–cardiomyocyte communication, and noncoding genomic enhancers. Together, these regulatory layers influence gene expression, cellular proliferation, metabolic reprogramming, and structural maturation, shaping the transition from fetal to mature cardiomyocytes.
Our laboratory integrates genetically engineered mouse models with human pluripotent stem cell-derived cardiomyocytes to dissect the molecular and cellular mechanisms underlying cardiac maturation. By investigating regulatory networks across transcriptional, post-transcriptional, and intercellular levels, we aim to understand how the heart acquires its mature functional identity and how disruptions to these processes contribute to cardiac disease.
How does the Tampakakis Lab investigate these processes?
Our research is made possible with the generous funds from:
