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)

An altered thyroid hormone profile has been reported in patients with congestive heart failure. However, information regarding the status of thyroid hormone receptors in human failing cardiomyocytes is lacking. Therefore the expression of thyroid hormone and beta-adrenergic receptors was investigated in human ventricular cardiomyocytes isolated from patients with end-stage heart failure (FM, n=12), or from tentative donors (C, n=4). The expression of thyroid (TRalpha1, and TRbeta1) and beta-adrenergic receptors (ARB1 and ARB2) was measured at both the gene, and at the protein level. In FM the reduced mRNA expression of ARB1 (p<0.05, -37%) and ARB2 (p<0.05, -42%) was associated with a reduction of the messenger for TRalpha1 (p<0.05, -85%) and TRalpha2 (p<0.05, -73%). These findings were confirmed at the protein level for ARB1, ARB2 and TRalpha1. These data reveal that in human heart failure the reduction of beta-adrenergic receptors is associated with reduced expression of both TRalpha1 and TRalpha2 isoforms of thyroid hormone receptors.
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PMID:Reduced expression of thyroid hormone receptors and beta-adrenergic receptors in human failing cardiomyocytes. 1803 13

It is well appreciated that several neurohormones and signaling cascades are activated that promote long-term deterioration of cardiac function and structure. Activation of the renin-angiotensin-aldosterone system (RAAS) and the adrenergic system is closely related to heart failure. Common gene variants that encode neurohormonal, adrenergic and intracellular proteins have been demonstrated to modulate the course and consequences of heart failure. However, the literature is replete with conflicting results and it remains uncertain as to whether particular gene variants predispose heart failure. Therefore, the main purpose of this review was to discuss the effects of single nucleotide polymorphisms (SNPs) that are located in genes encoding elements of the RAAS and the adrenergic system on the predisposition to and survival from heart failure. Most studies indicate that common SNPs encoding elements of the RAAS and the adrenergic system do not predispose individuals to heart failure. Conversely, it has been demonstrated that ARB1 Arg389Gly, GRK5 Gln41Leu, ACE I/D, CYP11B2 C-344T and AGTR1 A+1166C modulate pharmacological responses and have a considerable impact on cardiac-related survival. It should not be expected, however, that a single polymorphism determines survival, given that multiple gene products and environmental factors contribute to the pathogenesis of heart failure. Therefore, future studies should consider the interaction effects of multiple genes in populations that are as homogeneous as possible with respect to environmental characteristics.
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PMID:RAAS and adrenergic genes in heart failure: Function, predisposition and survival implications. 2116 Jul 50