RGD Reference Report - Proteomic analysis of early left ventricular hypertrophy secondary to hypertension: modulation by antihypertensive therapies. - Rat Genome Database

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Proteomic analysis of early left ventricular hypertrophy secondary to hypertension: modulation by antihypertensive therapies.

Authors: Gallego-Delgado, J  Lazaro, A  Osende, JI  Esteban, V  Barderas, MG  Gomez-Guerrero, C  Vega, R  Vivanco, F  Egido, J 
Citation: Gallego-Delgado J, etal., J Am Soc Nephrol. 2006 Dec;17(12 Suppl 3):S159-64.
RGD ID: 2313649
Pubmed: PMID:17130255   (View Abstract at PubMed)
DOI: DOI:10.1681/ASN.2006080937   (Journal Full-text)

Untreated or poorly controlled arterial hypertension induced development of pathologic left ventricular hypertrophy (LVH), a common finding in hypertensive patients and a strong predictor of cardiovascular morbidity and mortality. The proteomic approach is a powerful technique to analyze a complex mixture of proteins in various settings. An experimental model of hypertension-induced early LVH was performed in spontaneously hypertensive rats, and the cardiac protein pattern compared with the normotensive Wistar Kyoto counterpart was analyzed. Fifteen altered protein spots were shown in the early stage of LVH. Compared with a previous animal model of established and regressed LVH, three protein spots were common in both models. These three altered protein spots corresponded to two unique proteins that were identified as Calsarcin-1 (CS-1) and ubiquinone biosynthesis protein COQ7 homolog. CS-1 is a negative regulator of the calcineurin/NF-AT pathway. Because upregulation in the expression levels of this protein was observed, the activation level of NF-kappaB by oxidative stress as an alternative pathway was investigated. It was found that antihypertensive therapies partially decreased oxidative stress and normalized the activation of NF-kappaB in the kidneys and aorta NF-kappaB activation but just moderately in the heart. This could be due to the interaction of any specific cardiac protein with any component of the NF-kappaB pathway. In this sense, CS-1 could be a good candidate because it is expressed preferentially in heart, to a lesser extent in smooth muscle cells, but not in kidney. Further investigations are necessary to elucidate the exact role of CS-1 and ubiquinone biosynthesis protein COQ7 in the setting of hypertension-induced LVH.



RGD Manual Disease Annotations    Click to see Annotation Detail View
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
COQ7HumanLeft Ventricular Hypertrophy  ISOCoq7 (Rattus norvegicus)associated with Hypertension and protein:altered expression:heartRGD 
Coq7RatLeft Ventricular Hypertrophy  IEP associated with Hypertension and protein:altered expression:heartRGD 
Coq7MouseLeft Ventricular Hypertrophy  ISOCoq7 (Rattus norvegicus)associated with Hypertension and protein:altered expression:heartRGD 

Objects Annotated

Genes (Rattus norvegicus)
Coq7  (coenzyme Q7, hydroxylase)

Genes (Mus musculus)
Coq7  (demethyl-Q 7)

Genes (Homo sapiens)
COQ7  (coenzyme Q7, hydroxylase)


Additional Information