Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.1.2.13 (aldolase)
 3,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The metabolic changes in the homografted canine heart were studied in order to define the biochemical alterations accompanying homograft rejection. In several experiments, homograft rejection was accelerated by prior sensitization of the host animal. The homografted heart released pyruvate and lactate as well as malic dehydrogenase and aldolase. Extraction of glucose by the graft usually remained positive. During the accelerated rejection, the release of pyruvate and lactate was more pronounced, and even glucose appeared in increased concentrations in coronary vein blood. In many experiments the respiratory quotient of the transplanted heart as well as its glucose-oxygen extraction ratio were elevated. It seemed likely that the elevated respiratory quotients were the result of conversion of carbohydrates to fat, since the injection of thiamine hydrochloride resulted in further elevation of the respiratory quotient and in an increased myocardial pyruvate extraction. Apparently, thiamine corrected a metabolic block at the level of the cocarboxylase. The metabolic block or blocks present in the transplanted heart are likely to be the result of diminution in intracellular enzymes and coenzymes resulting from increased cellular permeability. The redox potential across the transplanted heart was positive, indicating the absence of anoxia. The results illustrate that glycolysis proceeds in the transplanted heart in the presence of oxygen. Histopathologic and histochemical studies show the earliest lesion to be an accumulation of lymphocytes around vessels at 3 hours. Swelling of vascular endothelium occurs. By 5 hours a polar perivascular cellular infiltrate of lymphocytes, plasma cells, macrophages, and histiocytes exists. Changes following at 19 hours show the appearance of Aschoff- and Anitschkow-like cells. Granulomatous myocarditis which was first perivascular became interstitial with lymphocytic and histiocytic invasion of the myocardium. After 8 days acceleration of swelling of vascular endothelium and granulomatous lesions were observed and necrosis of the myocardium was prominent. Endothelial hyperplasia occurred at 14 days. In the accelerated reaction these changes were intensified and necrosis began as early as 4 hours after grafting. Histochemical changes of DPNH diaphorase, lactic, malic, and succinic dehydrogenase showed only significant diminution of malic dehydrogenase in the cardiac muscle which was concurrent with the increase of this enzyme in the serum.
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PMID:Studies on the transplanted heart. Its metabolism and histology. 1387 18

A 57-year-old woman was admitted to our hospital because of a high fever, anemia, and hyperferritinemia. Since a bone marrow examination revealed hemophagocytosis, she was diagnosed with hemophagocytic syndrome (HPS). During treatment of HPS, a heliotrope rash and Gottron's sign appeared with elevated levels of serum aldolase. She also developed heart failure. She was diagnosed with dermatomyositis (DM) and associated myocarditis. Although the administration of glucocorticoids, calcineurin inhibitors, intravenous immunoglobulins, and etoposide ameliorated the clinical findings of DM and cytopenia, the fever and hyperferritinemia remained. The addition of infliximab to glucocorticoids and tacrolimus improved the fever and hyperferritinemia and enabled a reduction in the dose of prednisolone without relapse of the diseases.
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PMID:Hemophagocytic Syndrome Complicated with Dermatomyositis Controlled Successfully with Infliximab and Conventional Therapies. 2919 3

Acute myocarditis is an unpredictable heart disease that is caused by inflammation-associated cell death. Although viral infection and drug exposure are known to induce acute myocarditis, the molecular basis for its development remains undefined. Using proteomics and molecular analyses in myosin-induced rat experimental autoimmune myocarditis (EAM), we identified that elevated expression of aldolase 1A, retrogene 1 (Aldoart1) is critical to induce mitochondrial dysfunction and acute myocarditis development. Here, we demonstrate that cardiac cell death is associated with increased expressions of proapoptotic genes in addition to high levels of glucose, lactate, and triglyceride in metabolite profiling. The functional protein association network analysis also suggests that Aldoart1 upregulation correlates with high levels of dihydroxyacetone kinase and triglyceride. In H9c2 cardiac cells, lipopolysaccharides (LPS) or high glucose exposure significantly increases the cytochrome c release and the conversion of pro-caspase 3 into the cleaved form of caspase 3. We also found that LPS- or glucose-induced toxicities are almost completely reversed by siRNA-mediated knockdown of Aldoartl, which consequently increases cell viability. Together, our study strongly suggests that Aldoart1 may be involved in inducing mitochondrial apoptotic processes and can be a novel therapeutic target to prevent the onset of acute myocarditis or cardiac apoptosis.
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PMID:Elevated aldolase 1A, retrogene 1 expression induces cardiac apoptosis in rat experimental autoimmune myocarditis model. 3274 71