RGD Reference Report - Impairment of Cardiac Function and Remodeling Induced by Myocardial Infarction in Rats are Attenuated by the Nonpeptide Angiotensin-(1-7) Analog AVE 0991. - Rat Genome Database

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Impairment of Cardiac Function and Remodeling Induced by Myocardial Infarction in Rats are Attenuated by the Nonpeptide Angiotensin-(1-7) Analog AVE 0991.

Authors: Zeng, WT  Chen, WY  Leng, XY  Tang, LL  Sun, XT  Li, CL  Dai, G 
Citation: Zeng WT, etal., Cardiovasc Ther. 2010 Dec 19. doi: 10.1111/j.1755-5922.2010.00255.x.
RGD ID: 5129191
Pubmed: PMID:21167013   (View Abstract at PubMed)
DOI: DOI:10.1111/j.1755-5922.2010.00255.x   (Journal Full-text)

Aims: We evaluated effects of the nonpeptide angiotensin (ANG)-(1-7) analog AVE 0991 (AVE) on cardiac function and remodeling as well as transforming growth factor-beta1 (TGF-beta1)/tumor necrosis factor-alpha (TNF-alpha) expression in myocardial infarction rat models. Methods and Results: Sprague-Dawley rats underwent either sham surgery or coronary ligation. They were divided into four groups: sham, control, AVE, and AVE+A-779 [[D-Ala(7) ]-ANG-(1-7), a selective antagonist for the ANG-(1-7)] group. After 4 weeks of treatment, the AVE group displayed a significant elevation in left ventricular fractional shorting (LVFS) (25.5 +/- 7.3% vs. 18.4 +/- 3.3%, P < 0.05) and left ventricular ejection fraction (LVEF) (44.8 +/- 7.6% vs. 32.7 +/- 6.5%, P < 0.05) when compared to the control group, but no effects on the left ventricular end-diastolic and end-systolic diameters (LVDd and LVDs, respectively) were observed. In addition, we found that the myocyte diameter (18 +/- 2 mum vs. 22 +/- 4 mum, P < 0.05), infarct size (42.6 +/- 3.6% vs. 50.9 +/- 4.4%, P < 0.001) and collagen volume fraction (CVF) (16.4 +/- 2.2% vs. 25.3 +/- 3.2%, P < 0.001) were significantly reduced in the AVE group when compared to the control group. There were no differences in LVFS, LVEF, myocyte diameter, and infarct size between the control and AVE+A-779 groups. AVE also markedly attenuated the increased mRNA expression of collagen I (P < 0.001) and collagen III (P < 0.001) and inhibited the overexpression of TGF-beta1 (P < 0.05) and TNF-alpha (P < 0.05) compared to the control group. Conclusion: AVE could improve cardiac function and attenuate ventricular remodeling in MI rat models. It may involve the inhibition of inflammatory factors TGF-beta1/TNF-alpha overexpression and the action on the specific receptor Mas of ANG-(1-7).

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
myocardial infarction  ISOAgt (Rattus norvegicus)5129191; 5129191 RGD 
myocardial infarction  IDA 5129191 RGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
negative regulation of tissue remodeling  IDA 5129191 RGD 

Molecular Pathway Annotations    Click to see Annotation Detail View

RGD Manual Annotations

TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
myocardial infarction pathway  IDA 5129191 RGD 
Objects Annotated

Genes (Rattus norvegicus)
Agt  (angiotensinogen)

Genes (Mus musculus)
Agt  (angiotensinogen)

Genes (Homo sapiens)
AGT  (angiotensinogen)


Additional Information