Fibrosis is the formation or development of excess fibrous connective tissue (largely type I collagen) in a tissue as a result of a reparative or reactive process. Fibrosis, or scarring, is a common outcome in many chronic diseases of the heart, kidney, liver, lungs, or vasculature. Hepatic fibrosis is a result of chronic injury in response to insults such as viral hepatitis, alcohol or drug abuse, and increasingly from non-alcoholic steato hepatitis (NASH).[1] Fibrosis is a hallmark of end-stage renal disease.[2] Pulmonary fibrosis occurs in conditions such as chronic obstructive pulmonary disease.[3] Atherosclerosis involves vascular lesions with fibrous caps, and the thickness of this cap has been implicated in lesion (plaque) rupture resulting in thrombosis.[4] In the heart, hypertrophy from high blood pressure results in increased collagen levels.[5] Following heart attack, necrotic myocytes are replaced by extracellular matrix components, mainly collagen, to form a fibrotic myocardial scar.[6]

For all of these pathologies it would be useful to noninvasively detect, assess, and monitor fibrosis. Treatment decisions hinge on both the identity and severity of the disease. For instance NASH, which afflicts 1–2% of the US population, progresses to cirrhosis of the liver in about 20% of cases. Early detection and accurate characterization of liver fibrosis can improve patient outcomes.[7] Currently liver fibrosis is detected by liver biopsy, but biopsy is not wellsuited to screening/monitoring disease because of its cost,