Your browser doesn't support javascript.
loading
Chronic kidney disease mediates cardiac dysfunction associated with increased resident cardiac macrophages.
Mawhin, M A; Bright, R G; Fourre, J D; Vloumidi, E I; Tomlinson, J; Sardini, A; Pusey, C D; Woollard, K J.
Afiliación
  • Mawhin MA; Centre for Inflammatory Disease, Department of Immunology and Inflammation, Imperial College London, London, UK. m.mawhin@imperial.ac.uk.
  • Bright RG; Centre for Inflammatory Disease, Department of Immunology and Inflammation, Imperial College London, London, UK.
  • Fourre JD; Faculty of Medicine, National Heart & Lung Institute, Imperial College London, London, UK.
  • Vloumidi EI; MRC Laboratory of Molecular Biology, Imperial College London, London, UK.
  • Tomlinson J; Renal Directorate, Imperial College Healthcare NHS Trust, London, UK.
  • Sardini A; MRC London Institute of Medical Sciences, Imperial College London, London, UK.
  • Pusey CD; Centre for Inflammatory Disease, Department of Immunology and Inflammation, Imperial College London, London, UK.
  • Woollard KJ; Centre for Inflammatory Disease, Department of Immunology and Inflammation, Imperial College London, London, UK. k.woollard@imperial.ac.uk.
BMC Nephrol ; 23(1): 47, 2022 01 28.
Article en En | MEDLINE | ID: mdl-35090403
BACKGROUND: The leading cause of death in end-stage kidney disease is related to cardiovascular 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 less clear. 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 tested macrophage and chemokine implication in monocytopenic CCR2-/- and anti-CXCL10 treated mice. We quantified CXCL10 in human CKD plasma and tested the response of human iPSC-derived 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 monocytes contributed to this increase. We identified CXCL10 as a crucial factor for cardiac macrophage expansion in uremic disease. In humans, we found increased plasma CXCL10 concentrations in advanced CKD, and identified the production of CXCL10 in cardiomyocytes and cardiac fibroblasts. CONCLUSIONS: This study provides new insight into the role of the innate immune system in uremic cardiomyopathy.
Asunto(s)
Palabras clave
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Insuficiencia Renal Crónica / Corazón / Macrófagos / Miocardio Tipo de estudio: Prognostic_studies / Risk_factors_studies Límite: Animals Idioma: En Revista: BMC Nephrol Asunto de la revista: NEFROLOGIA Año: 2022 Tipo del documento: Article Pais de publicación: Reino Unido
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Insuficiencia Renal Crónica / Corazón / Macrófagos / Miocardio Tipo de estudio: Prognostic_studies / Risk_factors_studies Límite: Animals Idioma: En Revista: BMC Nephrol Asunto de la revista: NEFROLOGIA Año: 2022 Tipo del documento: Article Pais de publicación: Reino Unido