The insulin-like growth factor family: molecular mechanisms, redox regulation, and clinical implications.

Insulin-like growth factor (IGF)-induced signaling networks are vital in modulating multiple fundamental cellular processes, such as cell growth, survival, proliferation, and differentiation. Aberrations in the generation or action of IGF have been suggested to play an important role in several pathological conditions, including metabolic disorders, neurodegenerative diseases, and multiple types of cancer. Yet the exact mechanism involved in the pathogenesis of these diseases by IGFs remains obscure. Redox pathways involving reactive oxygen species (ROS) and reactive nitrogen species (RNS) contribute to the pathogenetic mechanism of various diseases by modifying key signaling pathways involved in cell growth, proliferation, survival, and apoptosis. Furthermore, ROS and RNS have been demonstrated to alter IGF production and/or action, and vice versa, and thereby have the ability to modulate cellular functions, leading to clinical manifestations of diseases. In this review, we provide an overview on the IGF system and discuss the potential role of IGF-1/IGF-1 receptor and redox pathways in the pathophysiology of several diseases.