Mediation of cardioprotection by transforming growth factor-B

Ischemic heart disease is caused by the lack of oxygen in the tissues of the heart. Free radicals derived from oxygen, such as superoxide anions, and various cellular factors, such as the cytokines, interleukin-1 and tumor necrosis factor, are thought to mediate the damage to the heart muscle. These cellular factors are released by the neutrophil, a type of white blood cell, and by endothelial cells, cells that line the heart and blood vessels. The effects of these factors can be counteracted by another factor, known as transforming growth factor-beta (TGF-beta). TGF-beta can cause normal fibroblastic cells to transform into cancerous cells. It has been shown that TGF-beta is involved in the regulation of a number of processes involved in development. TGF-beta is present in heart cells and in the endothelial cells. TGF-beta inhibits neutrophils from adhering to endothelial cells and may therefore moderate the effects of ischemia. The ability of TGF to protect the heart tissue after ischemia was studied. TGF-beta was shown to reduce the amounts of superoxide anions, prevent the small blood vessels of the heart from dilating, and reduce injury when tumor necrosis factor was introduced to the heart cells. If administered within a short period of time after a heart attack, which was experimentally induced in rats, TGF-beta reduced the amount of injury which occurred to the heart cells. TGF-beta produced by genetic engineering is available, and can potentially be used as a therapeutic agent after heart attack. (Consumer Summary produced by Reliance Medical Information, Inc.)