Abstract
Titin is the largest known protein in the human body and operates as a signaling hub, contributes to passive force in the muscle, and as a molecular spring. Muscle tissue experiences damage and atrophy for many reasons including exercise, disease, or age. When muscle tissue is catabolized, a consistent biomarker can be found in the urine: urinary titin N-terminal fragment (UTF). This biomarker was first identified in 2014, but research into this biomarker began in earnest in 2016 when UTF was found to be elevated in both Duchenne muscular dystrophy patients and individuals post-exercise compared to the control groups. Subsequent research found that while Duchenne muscular dystrophy has increased UTF values, this symptom is common across many muscular dystrophy disorders. It's been postulated that UTF values could be an effective diagnostic tool for early muscular dystrophy disorders and certain forms of myopathy. Both muscle atrophy and eccentric exercise have both been shown to produce elevated UTF as well. This review highlights the key findings over the past 10 years in this field and identifies questions regarding production of UTF that should be the focus of the next 10 years of work in this area.