An etiologic basis for congestive heart failure on the molecular level.
It is here proposed that disordered redox balance leads to congestive heart failure in a variety of diverse clinical situations. These conditions include those associated with an excess of reducing agents, such as catecholamines and thyroid hormone, or impaired oxidant defenses, such as in selenium deficiency. The clinical situations include hypertension, hyperthyroidism, progressive congestive heart failure, amphetamine overdose and hemochromatosis. The molecular damage to the cardiac muscle is postulated to be mediated via reaction oxygen radicals.
D005609:Free Radicals; D006333:Heart Failure / Q000378:metabolism*; D006801:Humans; D007501:Iron / Q000378:metabolism; D007511:Ischemia / Q000378:metabolism; D008954:Models, Biological; D010084:Oxidation-Reduction; D010100:Oxygen / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism*
D005609:Free Radicals; D013481:Superoxides; D007501:Iron; D010100:Oxygen