RESUMO
Tumor necrosis factor (TNF) is a proinflammatory cytokine that can produce widespread deleterious effects when expressed in large amounts. It is produced in the heart by both cardiac myocytes and resident macrophages under conditions of cardiac stress, and is thought to be responsible for many of the untoward manifestations of cardiac disease. This article discusses the role of TNF in heart disease and some potential therapeutic modalities that can influence the cytokine activity. The results of controlled studies would suggest that TNF inhibition does not influence the clinical course of patients with heart failure.
Assuntos
Cardiopatias/fisiopatologia , Fator de Necrose Tumoral alfa/fisiologia , Animais , Biomarcadores/sangue , Ensaios Clínicos como Assunto , Cardiopatias/sangue , Humanos , Receptores do Fator de Necrose Tumoral/metabolismo , Transdução de Sinais/fisiologia , Fator de Necrose Tumoral alfa/uso terapêuticoRESUMO
L-carnitine and its derivative, propionyl-L-carnitine, are organic amines produced and metabolized endogenously. These compounds are essential in the process of fatty acid oxidation and have also been shown to reduce intracellular accumulation of toxic metabolites during ischemia. Currently, exogenous administration of carnitine is indicated only as therapy for primary and secondary carnitine deficiency. However, it has been hypothesized that because of its ability to enhance energy production and remove toxic metabolites during ischemia, carnitine therapy may be useful in the treatment of various cardiac diseases. In fact, there is increasing evidence that endogenous carnitine has beneficial effects in the treatment of congestive heart failure, arrhythmia, peripheral vascular disease, and acute ischemia.