The ability to impede/reduce complication of the damaged heart presents a major challenge in the treatment of cardiovascular diseases. Complications include heart failure, which has a high mortality even with current treatments. The use of a new drug to stimulate protection of the heart during an ongoing myocardial infarct and long term changes leading to heart failure would be very relevant to the clinical setting, to help patients suffering from diverse heart problems.
Heart failure (HF) is a condition that develops after the heart becomes damaged or weakened. HF occurs when the pumping action of the heart is not strong enough to move blood around, especially during increased activity or under stress. In addition, the heart muscle may not relax properly to accommodate the flow of blood back from the lungs to the heart. These abnormalities in heart function can cause fluid to back up in lungs and in other parts of body.
Fibroproliferative disorders are a/the leading cause of morbidity and mortality worldwide. A large group of interstitial lung diseases (ILD) can cause progressive scarring of lung tissues, affecting the ability to breathe. Idiopathic Pulmonary Fibrosis (IPF) is one of the major forms of ILD and is characterized by a progressive decline in lung function. Although the pathogenesis of IPF is incompletely understood, work from our group and others suggest that transforming growth factor beta 1 (TGF-?1) is involved in the fibrogenic process.