RGD Reference Report - Myocardial infarction impairs renal function, induces renal interstitial fibrosis, and increases renal KIM-1 expression: implications for cardiorenal syndrome. - Rat Genome Database

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Myocardial infarction impairs renal function, induces renal interstitial fibrosis, and increases renal KIM-1 expression: implications for cardiorenal syndrome.

Authors: Lekawanvijit, S  Kompa, AR  Zhang, Y  Wang, BH  Kelly, DJ  Krum, H 
Citation: Lekawanvijit S, etal., Am J Physiol Heart Circ Physiol. 2012 May 1;302(9):H1884-93. doi: 10.¿1152/¿ajpheart.¿00967.¿2011. Epub 2012 Feb 24.
RGD ID: 7245950
Pubmed: PMID:22367506   (View Abstract at PubMed)
DOI: DOI:10.1152/ajpheart.00967.2011   (Journal Full-text)

Progressive decline in renal function coexists with myocardial infarction (MI); however, little is known about its pathophysiology. This study aimed to systematically identify post-MI renal changes (functional, histological, and molecular) over time in a rat MI model and examine potential mechanisms that may underlie these changes. Rats were randomized into three groups: nonoperated, sham, and MI. Cardiac and renal function was assessed before death at 1, 4, 8, 12, and 16 wk with tissues collected for histological, protein, and gene studies. Tail-cuff blood pressure was lower in MI than sham and nonoperated animals only at 1 wk (P < 0.05). Systolic function was reduced (P < 0.0001) while heart/body weight and left ventricle/body weight were significantly greater in MI animals at all time points. Glomerular filtration rate decreased following MI at 1 and 4 wk (P < 0.05) but not at 8 and 12 wk and then deteriorated further at 16 wk (P = 0.052). Increased IL-6 gene and transforming growth factor (TGF)-beta protein expression as well as macrophage infiltration in kidney cortex was detected at 1 wk (P < 0.05). Renal cortical interstitial fibrosis was significantly greater in MI animals from 4 wk, while TGF-beta bioactivity (phospho-Smad2) was upregulated at all time points. The degree of fibrosis increased and was maximal at 16 wk. In addition, kidney injury molecule-1-positive staining in the tubules was more prominent in MI animals, maximal at 1 wk. In conclusion, renal impairment occurs early post-MI and is associated with hemodynamic and structural changes in the kidney possibly via activation of the Smad2 signaling pathway.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
HAVCR1HumanCardio-Renal Syndrome  ISOHavcr1 (Rattus norvegicus)protein:increased expression:kidney tubule:RGD 
Havcr1RatCardio-Renal Syndrome  IEP protein:increased expression:kidney tubule:RGD 
Havcr1MouseCardio-Renal Syndrome  ISOHavcr1 (Rattus norvegicus)protein:increased expression:kidney tubule:RGD 

Objects Annotated

Genes (Rattus norvegicus)
Havcr1  (hepatitis A virus cellular receptor 1)

Genes (Mus musculus)
Havcr1  (hepatitis A virus cellular receptor 1)

Genes (Homo sapiens)
HAVCR1  (hepatitis A virus cellular receptor 1)


Additional Information