In this section
@article{Woollard:2022:10.1186/s12882-021-02593-7,
author = {Woollard, K},
doi = {10.1186/s12882-021-02593-7},
journal = {BMC Nephrology},
pages = {1--15},
title = {Chronic kidney disease mediates cardiac dysfunction associated with increased resident cardiac macrophages},
url = {http://dx.doi.org/10.1186/s12882-021-02593-7},
volume = {23},
year = {2022}
}
TY - JOUR
AB - Background – The leading cause of death in end-stage kidney disease is related tocardiovascular disease. Macrophages are known to be involved in both chronic kidney disease(CKD) and heart failure, however their role in the development of cardiorenal syndrome is lessclear. We thus sought to investigate the role of macrophages in uremic cardiac disease.Methods – We assessed cardiac response in two experimental models of CKD and testedmacrophage and chemokine implication in monocytopenic CCR2-/- and anti-CXCL10 treatedmice. We quantified CXCL10 in human CKD plasma and tested the response of human iPSCderived cardiomyocytes and primary cardiac fibroblasts to serum from CKD donors. Results– We found that reduced kidney function resulted in the expansion of cardiac macrophages,in particular through local proliferation of resident populations. Influx of circulating monocytescontributed to this increase. We identified CXCL10 as a crucial factor for cardiac macrophageexpansion in uremic disease. In humans, we found increased plasma CXCL10 concentrationsin advanced CKD, and identified the production of CXCL10 in cardiomyocytes and cardiacfibroblasts. Conclusions – This study provides new insight into the role of the innate immunesystem in uremic cardiomyopathy.
AU - Woollard,K
DO - 10.1186/s12882-021-02593-7
EP - 15
PY - 2022///
SN - 1471-2369
SP - 1
TI - Chronic kidney disease mediates cardiac dysfunction associated with increased resident cardiac macrophages
T2 - BMC Nephrology
UR - http://dx.doi.org/10.1186/s12882-021-02593-7
UR - https://bmcnephrol.biomedcentral.com/articles/10.1186/s12882-021-02593-7
UR - http://hdl.handle.net/10044/1/92823
VL - 23
ER -
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