Serelaxin attenuates renal inflammation and fibrosis in a mouse model of dilated cardiomyopathy
Beverly Giam, Po-Yin Chu, Sanjaya Kuruppu, A. Ian Smith, Duncan Horlock, Aishwarya Murali, Helen Kiriazis, Xiao-Jun Du, David M. Kaye, Niwanthi W. Rajpakse
Experimental Physiology; 2018; 103(12): 1593-1602
Beverly Giam (Australia)
Published work: ‘Serelaxin attenuates renal inflammation and fibrosis in a mouse model of dilated cardiomyopathy’ in Experimental Physiology
1) Summarise your work in one sentence.
We sought to determine the renoprotective effects of serelaxin in the setting of heart failure.
2) Summarise your findings in one sentence.
Treatment with serelaxin can attenuate the development of renal fibrosis in mice with dilated cardiomyopathy, and this is likely to be mediated, at least in part, via a reduction in the renal expression of pro-inflammatory markers Tnfa and Il1a.
3) Which were the more important methods you used in this work? If it is not a traditional method you can briefly explain the concept of that methodology.
Quantification of inflammatory related genes in the renal cortical region via qPCR indicate that mice with dilated cardiomyopathy had greater levels of inflammation compared to WT mice, and treatment with serelaxin reduced renal cortical levels of inflammation in the former genotype compared to vehicle treated controls.
Assessment of renal fibrosis via Masson’s Trichrome stain indicate that mice with dilated cardiomyopathy had greater levels of renal tubulointerstitial and glomerular fibrosis compared to WT mice. Treatment with serelaxin attenuated renal fibrosis in the former genotype compared to vehicle treated controls.
4) What did you learn from this paper, what was your take-home message?
Our data indicate that serelaxin has the potential to target renal inflammation and fibrosis in the setting of established cardiac dysfunction. These findings provide a basis to further investigate the renoprotective effects of serelaxin in chronic heart failure.