RGD Reference Report - Cardioprotective effects of telmisartan against heart failure in rats induced by experimental autoimmune myocarditis through the modulation of angiotensin-converting enzyme-2/angiotensin 1-7/mas receptor axis. - Rat Genome Database

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Cardioprotective effects of telmisartan against heart failure in rats induced by experimental autoimmune myocarditis through the modulation of angiotensin-converting enzyme-2/angiotensin 1-7/mas receptor axis.

Authors: Sukumaran, V  Veeraveedu, PT  Gurusamy, N  Yamaguchi, K  Lakshmanan, AP  Ma, M  Suzuki, K  Kodama, M  Watanabe, K 
Citation: Sukumaran V, etal., Int J Biol Sci. 2011;7(8):1077-92. Epub 2011 Sep 8.
RGD ID: 5685668
Pubmed: PMID:21927577   (View Abstract at PubMed)
PMCID: PMC3174385   (View Article at PubMed Central)

Angiotensin-converting enzyme-2 (ACE-2) is a homolog of ACE that preferentially forms angiotensin-(ANG)-1-7 from angiotensin II (ANG II). We investigated the cardioprotective effects of telmisartan, a well-known angiotensin receptor blockers (ARBs) against experimental autoimmune myocarditis (EAM). EAM was induced in Lewis rats by immunization with porcine cardiac myosin. The rats were divided into two groups and treated with telmisartan (10 mg/kg/day) or vehicle for 21 days. Myocardial functional parameters were significantly improved by treatment with telmisartan compared with vehicle-treated rats. Telmisartan lowered myocardial protein expressions of NADPH oxidase subunits 3-nitrotyrosine, p47phox, p67 phox, Nox-4 and superoxide production significantly than vehicle-treated rats. In contrast myocardial protein levels of ACE-2, ANG 1-7 mas receptor were upregulated in the telmisartan treated group compared with those of vehicle-treated rats. The myocardial protein expression levels of tumor necrosis factor receptor (TNFR)-associated factor (TRAF)-2, C/EBP homologous protein (CHOP) and glucose-regulated protein (GRP) 78 were decreased in the telmisartan treated rats compared with those of vehicle-treated rats. In addition, telmisartan treatment significantly decreased the protein expression levels of phospho-p38 mitogen-activated protein kinase (MAPK), phospho-JNK, phospho-ERK and phospho (MAPK) activated protein kinase-2 than with those of vehicle-treated rats. Moreover, telmisartan significantly decreased the production of proinflammatory cytokines, myocardial apoptotic markers and caspase-3 positive cells compared with those of vehicle-treated rats. Therefore, we suggest that telmisartan was beneficial protection against heart failure in rats, at least in part by suppressing inflammation, oxidative stress, ER stress as well as signaling pathways through the modulation of ACE2/ANG1-7/Mas receptor axis.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
HSPA5HumanExperimental Autoimmune Myocarditis treatmentISOHspa5 (Rattus norvegicus) RGD 
Hspa5RatExperimental Autoimmune Myocarditis treatmentIEP  RGD 
Hspa5MouseExperimental Autoimmune Myocarditis treatmentISOHspa5 (Rattus norvegicus) RGD 

Objects Annotated

Genes (Rattus norvegicus)
Hspa5  (heat shock protein family A (Hsp70) member 5)

Genes (Mus musculus)
Hspa5  (heat shock protein 5)

Genes (Homo sapiens)
HSPA5  (heat shock protein family A (Hsp70) member 5)


Additional Information