Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The adenine nucleotide translocator (ANT), the only mitochondrial carrier for ADP and ATP, combines mitochondrial energy-producing and cytosolic energy-consuming processes. The ANT function was observed to be impaired in explanted heart tissue from patients with dilated cardiomyopathy (DCM). In order to clarify whether an altered ANT isoform composition might be responsible for the restricted ANT function, we analyzed the ANT isoform expression pattern in the myocardium of patients suffering from dilated cardiomyopathy. The ANT isoform mRNA pattern was analyzed in explanted hearts from patients with dilated cardiomyopathy (n = 29), ischemic (n = 22) and valvular cardiomyopathy (n = 7) using the polymerase chain reaction technique. Myocardium from 12 subjects without heart disease was used as control. In addition, right ventricular biopsies from 47 patients with dilated cardiomyopathy who underwent cardiac catheterization were tested. A shift in the ANT isoform transcription profile was found in heart tissue from patients with dilated cardiomyopathy, but not in those from patients with ischemic or valvular cardiomyopathy. The shift was characterized by an increase in the ANT1 mRNA percentage, a decrease in ANT2 and an unchanged ANT3 proportion. Both ventricles and the septum were affected by the shift. The alteration was also found in endomyocardial specimens taken from patients with ongoing dilated cardiomyopathy. An alteration in the ANT isoform pattern was found to be specific for dilated cardiomyopathy. It is not a general phenomenon of end-stage heart failure, but occurs already before the heart is finally damaged. Therefore, an altered ANT isoform expression appears to be a feature of a dilated cardiomyopathy-specific gene program.
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PMID:The myocardial expression of the adenine nucleotide translocator isoforms is specifically altered in dilated cardiomyopathy. 1090 36

Little is known about the right ventricular (RV) proteome in human heart failure (HF), including possible differences compared to the left ventricular (LV) proteome. We used 2-dimensional differential in-gel electrophoresis (pH: 4-7, 10-150 kDa), followed by liquid chromatography tandem mass spectrometry, to compare the RV and LV proteomes in 12 explanted human hearts. We used Western blotting and multiple-reaction monitoring for protein verification and RNA sequencing for messenger RNA and protein expression correlation. In all 12 hearts, the right ventricles (RVs) demonstrated differential expression of 11 proteins relative to the left ventricles (LVs), including lesser expression of CRYM, TPM1, CLU, TXNL1, and COQ9 and greater expression of TNNI3, SAAI, ERP29, ACTN2, HSPB2, and NDUFS3. Principal-components analysis did not suggest RV-versus-LV proteome partitioning. In the nonischemic RVs (n = 6), 7 proteins were differentially expressed relative to the ischemic RVs (n = 6), including increased expression of CRYM, B7Z964, desmin, ANXA5, and MIME and decreased expression of SERPINA1 and ANT3. Principal-components analysis demonstrated partitioning of the nonischemic and ischemic RV proteomes, and gene ontology analysis identified differences in hemostasis and atherosclerosis-associated networks. There were no proteomic differences between RVs with echocardiographic dysfunction (n = 8) and those with normal function (n = 4). Messenger RNA and protein expression did not correlate consistently, suggesting a major role for RV posttranscriptional protein expression regulation. Differences in contractile, cytoskeletal, metabolic, signaling, and survival pathways exist between the RV and the LV in HF and may be related to the underlying HF etiology and differential posttranscriptional regulation.
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PMID:Right ventricular protein expression profile in end-stage heart failure. 2640 Dec 49