RGD Reference Report - Adiponectin expression in patients with inflammatory cardiomyopathy indicates favourable outcome and inflammation control. - Rat Genome Database

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Adiponectin expression in patients with inflammatory cardiomyopathy indicates favourable outcome and inflammation control.

Authors: Bobbert, P  Scheibenbogen, C  Jenke, A  Kania, G  Wilk, S  Krohn, S  Stehr, J  Kuehl, U  Rauch, U  Eriksson, U  Schultheiss, HP  Poller, W  Skurk, C 
Citation: Bobbert P, etal., Eur Heart J. 2011 May;32(9):1134-47. Epub 2011 Jan 29.
RGD ID: 5686895
Pubmed: PMID:21278397   (View Abstract at PubMed)
DOI: DOI:10.1093/eurheartj/ehq498   (Journal Full-text)

AIMS: Circulating adiponectin (APN) is an immunomodulatory, pro-angiogenic, and anti-apoptotic adipocytokine protecting against acute viral heart disease and preventing pathological remodelling after cardiac injury. The purpose of this study was to describe the regulation and effects of APN in patients with inflammatory cardiomyopathy (DCMi). METHODS AND RESULTS: Adiponectin expression and outcome were assessed in 173 patients with DCMi, 30 patients with non-inflammatory DCM, and 30 controls. Mechanistic background of these findings was addressed in murine experimental autoimmune myocarditis (EAM), a model of human DCMi, and further elucidated in vitro. Adiponectin plasma concentrations were significantly higher in DCMi compared with DCM or controls, i.e. 6.8 +/- 3.9 microg/mL vs. 5.4 +/- 3.6 vs. 4.76 +/- 2.5 microg/mL (P< 0.05, respectively) and correlated significantly with cardiac mononuclear infiltrates (CD3+: r(2)= 0.025, P= 0.038; CD45R0+: r(2)= 0.058, P= 0.018). At follow-up, DCMi patients with high APN levels showed significantly increased left ventricular ejection fraction improvement, decreased left ventricular end-diastolic diameter, and reduced cardiac inflammatory infiltrates compared with patients with low APN levels. A multivariate linear regression analysis implicated APN as an independent prognostic factor for inhibition of cardiac inflammation. In accordance with these findings in human DCMi, EAM mice exhibited elevated plasma APN. Adiponectin gene transfer led to significant downregulation of key inflammatory mediators promoting disease. Mechanistically, APN acted as a negative regulator of T cells by reducing antigen specific expansion (P< 0.01) and suppressed TNFalpha-mediated NFkappaB activation (P< 0.01) as well as release of reactive oxygen species in cardiomyocytes. CONCLUSION: Our results implicate that APN acts as endogenously upregulated anti-inflammatory cytokine confining cardiac inflammation and progression in DCMi.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
cardiomyopathy disease_progressionIEP 5686895associated with inflammation more ...RGD 
cardiomyopathy disease_progressionISOADIPOQ (Homo sapiens)5686895; 5686895associated with inflammation more ...RGD 
myocarditis  ISOAdipoq (Mus musculus)5686895; 5686895mRNA more ...RGD 
myocarditis  IMP 5686895mRNA more ...RGD 

Objects Annotated

Genes (Rattus norvegicus)
Adipoq  (adiponectin, C1Q and collagen domain containing)

Genes (Mus musculus)
Adipoq  (adiponectin, C1Q and collagen domain containing)

Genes (Homo sapiens)
ADIPOQ  (adiponectin, C1Q and collagen domain containing)


Additional Information