Abstract

Transforming growth factor beta-1 is involved in local signaling for avariety of human diseases including renal diseases, cardiac hypertrophy and fibrosis in heart failure,hepatic fibrosis, and pulmonary fibrosis. Elevated levels of circulating transforming growth factor beta-1result in organ fibrosis in animal models. In humans smoking, hypertension, diabetes and obesity appearto result in elevated circulating levels. This paper outlines a hypothesis that elevated circulatinglevels of transforming growth factor beta-1 are part of the molecular link between several entities thathave epidemiologic ties including hypertension, diabetes, smoking and obesity on one hand and diseasesresulting in organ fibrosis on the other including renal disease and cardiac fibrosis and hypertrophyin heart failure. Additionally, it is suggested that elevated levels are not simply a marker of a similarmechanism of disease production but that elevated levels of circulating transforming growth factor beta-1lead to disease production and to the synergy of risk factors seen in production of human fibrotic diseases.

Keywords: Obesity - metabolism, Diabetes Mellitus - metabolism, Fibrosis - metabolism, Hypertension - metabolism, Models, Animal, Obesity - metabolism, Smoking, Transforming Growth Factor beta - physiology, Transforming Growth Factor beta1