Our laboratory investigates the molecular mechanisms that regulate skeletal muscle formation, regeneration, and degeneration. A central focus of our work is understanding how these mechanisms are altered in musculoskeletal diseases, particularly muscular dystrophies. A key component of our research is the extracellular matrix (ECM)—the structural environment that surrounds muscle cells and plays a critical role in muscle development and repair. When the ECM becomes dysregulated, it can lead to muscle fibrosis, a pathological accumulation of matrix components that progressively impairs muscle function. Muscle fibrosis is a hallmark of several conditions, including Duchenne muscular dystrophy (DMD), motor neuron diseases such as ALS, and age-associated sarcopenia. Our research explores the signaling pathways that drive this fibrotic process, including TGF-β, CTGF/CCN2, elements of the renin–angiotensin system, and lysophosphatidic acid (LPA). We are also investigating the cell populations responsible for fibrosis in different muscle injury and disease models, with the goal of identifying new therapeutic targets. Importantly, our laboratory has identified inhibitors of key profibrotic pathways that significantly improve muscle pathology in experimental models. Several of these strategies have advanced to human clinical trials (Phase II and Phase III), highlighting the translational potential of our work. Our ultimate goal is to translate molecular discoveries into therapies that improve muscle health and quality of life for patients with neuromuscular diseases.