Mediation of cardioprotection by transforming growth factor-B
Article Abstract:
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.)
Publication Name: Science
Subject: Science and technology
ISSN: 0036-8075
Year: 1990
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The mysteries of lipoprotein(a)
Article Abstract:
Lipoprotein(a)-Lp(a) is a molecule found in the blood plasma. Lp(a) is a complex of low-density lipoprotein (LDL) and apolipoprotein(a)-apo(a). LDLs are the major transporters of cholesterol in human plasma. Apo(a) is similar to plasminogen, a molecule that binds to fibrin molecules present in blood clots and causes the dissolution of the clot. It is thought that due to the similarity of Lp(a) and plasminogen, Lp(a) may also bind to fibrin. Cholesterol, therefore, may be transported by Lp(a) to damaged arteries that have been recently repaired by blood clots. High levels of Lp(a) are associated with premature heart disease and stroke. Individuals who have Lp(a) concentrations greater than 50 milligrams per deciliter of plasma and high LDL concentrations may have up to a six-fold higher risk for early heart disease and arteriosclerosis, or hardening of the arteries. The concentration of Lp(a) in plasma of individuals varies greatly, by three orders of magnitude. The variation in plasma levels of Lp(a) is under genetic control. Major differences in the concentrations of Lp(a) are seen in different ethnic groups. Additional studies are being carried out to understand the function of Lp(a), how the molecule is assembled and destroyed, the evolution of Lp(a), and how the concentrations in the plasma are regulated. The understanding of Lp(a) and its involvement in disease may lead to the diagnosis, prevention or treatment of heart disease.
Publication Name: Science
Subject: Science and technology
ISSN: 0036-8075
Year: 1989
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Heart attacks: gone with the century?
Article Abstract:
Coronary disease may not be a major public health problem in the 21st century due to recent scientific breakthroughs. Research clearly shows that LDL cholesterol and heart disease are linked. Progress in the study of drugs called statins and genetic susceptibility factors is also discussed.
Publication Name: Science
Subject: Science and technology
ISSN: 0036-8075
Year: 1996
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