Our work investigates how metabolic pathways sustain skeletal muscle health and neuromuscular communication. The AKT signaling pathway, a central regulator of muscle growth and performance, is indispensable for maintaining muscle mass and function. Preliminary findings from our lab reveal that insulin-driven AKT signaling plays a critical role in stabilizing NMJ structure—the key site of communication between motor neurons and muscle fibers. Using RNA in situ hybridization to track acetylcholine receptor (AChR) turnover, alongside gene therapy approaches, we aim to uncover how AKT-regulated molecules preserve NMJ integrity. These insights may open new therapeutic avenues for sarcopenia, insulin resistance, and neuromuscular disorders.

Skeletal muscle insulin resistance is a defining feature of metabolic diseases such as obesity and type 2 diabetes, particularly in aging populations. Sarcopenia—the progressive decline in muscle mass and strength—becomes even more detrimental when combined with obesity, leading to sarcopenic obesity. This condition poses a major public health challenge, reducing mobility, metabolic health, and overall lifespan. Through genetic mouse models and human translational studies, we employ single-cell transcriptomics, phosphoproteomics, and metabolic profiling to dissect the molecular pathways that safeguard lean mass in obesity and aging.

Emerging evidence suggests that the gut microbiome profoundly influences muscle physiology through metabolites, inflammatory signals, and gut-derived hormones. Our lab is pioneering studies on the gut-muscle axis to understand how microbiome composition shapes muscle strength, insulin sensitivity, and metabolic flexibility. This research highlights the microbiome as a potential target for improving muscle health and metabolic outcomes.

Mitochondria are central to energy production and cellular resilience. Dysfunction in these organelles contributes to a wide range of health conditions. This project focuses on unraveling the mechanisms of mitochondrial impairment across both healthy and disease states, with the goal of identifying strategies to preserve mitochondrial function and enhance overall metabolic health.