RGD Reference Report - Myocardin ablation in a cardiac-renal rat model. - Rat Genome Database

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Myocardin ablation in a cardiac-renal rat model.

Authors: Mittal, Anupam  Rana, Santanu  Sharma, Rajni  Kumar, Akhilesh  Prasad, Rishikesh  Raut, Satish K  Sarkar, Sagartirtha  Saikia, Uma Nahar  Bahl, Ajay  Dhandapany, Perundurai S  Khullar, Madhu 
Citation: Mittal A, etal., Sci Rep. 2019 Apr 10;9(1):5872. doi: 10.1038/s41598-019-42009-z.
RGD ID: 401793740
Pubmed: PMID:30971740   (View Abstract at PubMed)
PMCID: PMC6458122   (View Article at PubMed Central)
DOI: DOI:10.1038/s41598-019-42009-z   (Journal Full-text)

Cardiorenal syndrome is defined by primary heart failure conditions influencing or leading to renal injury or dysfunction. Dilated cardiomyopathy (DCM) is a major co-existing form of heart failure (HF) with renal diseases. Myocardin (MYOCD), a cardiac-specific co-activator of serum response factor (SRF), is increased in DCM porcine and patient cardiac tissues and plays a crucial role in the pathophysiology of DCM. Inhibiting the increased MYOCD has shown to be partially rescuing the DCM phenotype in porcine model. However, expression levels of MYOCD in the cardiac tissues of the cardiorenal syndromic patients and the effect of inhibiting MYOCD in a cardiorenal syndrome model remains to be explored. Here, we analyzed the expression levels of MYOCD in the DCM patients with and without renal diseases. We also explored, whether cardiac specific silencing of MYOCD expression could ameliorate the cardiac remodeling and improve cardiac function in a renal artery ligated rat model (RAL). We observed an increase in MYOCD levels in the endomyocardial biopsies of DCM patients associated with renal failure compared to DCM alone. Silencing of MYOCD in RAL rats by a cardiac homing peptide conjugated MYOCD siRNA resulted in attenuation of cardiac hypertrophy, fibrosis and restoration of the left ventricular functions. Our data suggest hyper-activation of MYOCD in the pathogenesis of the cardiorenal failure cases. Also, MYOCD silencing showed beneficial effects by rescuing cardiac hypertrophy, fibrosis, size and function in a cardiorenal rat model.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Cardio-Renal Syndrome amelioratesISOMyocd (Rattus norvegicus)401793740; 401793740 RGD 
Cardio-Renal Syndrome  IEP 401793740mRNA and protein:increased expression:left ventricleRGD 
Cardio-Renal Syndrome amelioratesIMP 401793740 RGD 
Cardio-Renal Syndrome  ISOMYOCD (Homo sapiens)401793740; 401793740mRNA and protein:increased expression:left ventricleRGD 

Objects Annotated

Genes (Rattus norvegicus)
Myocd  (myocardin)

Genes (Mus musculus)
Myocd  (myocardin)

Genes (Homo sapiens)
MYOCD  (myocardin)

Additional Information