The central question driving the laboratory is simple: why does the mammalian heart lose its ability to regenerate? In the days following birth, cardiomyocytes permanently exit the cell cycle, a transition that, once complete, leaves the adult heart without capacity for self-repair. Understanding the molecular logic of this transition, and finding ways to reverse it, is what the laboratory is built around.

Our research focuses on the pathways that govern cardiomyocyte cell-cycle arrest and re-entry. Key areas of investigation include the transcriptional regulators MEIS1 and HOXB13, calcineurin signaling, sarcomere remodeling, and innate immune pathways, particularly the cGAS–STING axis, which has emerged as an important player in cardiac regenerative biology. The laboratory uses mouse genetic models, human iPSC-derived cardiomyocytes, genomic approaches, and advanced imaging to dissect how these mechanisms interact and collectively determine regenerative potential.

A parallel effort focuses on the development of experimental platforms that allow dynamic, real-time analysis of cardiomyocyte proliferation, maturation, and structural remodeling in human cellular systems. These tools are essential for addressing one of the field's core challenges: how to drive cell-cycle re-entry without compromising the contractile function that keeps the heart working.

The longer-term objective is translation. Current projects are identifying novel molecular targets and testing pharmacological and genetic strategies to stimulate myocardial repair in the context of heart failure. The laboratory works at the intersection of basic biology and therapeutic development, close enough to the clinic to stay oriented, far enough from it to ask questions that don't yet have answers.