title: Macrophage in chronic kidney disease.
abstract: Chronic kidney disease (CKD) has become a major health problem worldwide. This review describes the role of macrophages in CKD and highlights the importance of anti-inflammatory M2 macrophage activation in both renal fibrosis and wound healing processes. Furthermore, the mechanisms by which M2 macrophages induce renal repair and regeneration are still under debate and currently demand more attention. The M1/M2 macrophage balance is related to the renal microenvironment and could influence CKD progression. In fact, an inflammatory renal environment and M2 plasticity can be the major hurdles to establishing macrophage cell-based therapies in CKD. M2 macrophage cell-based therapy is promising if the M2 phenotype remains stable and is 'fixed' byin vitromanipulation. However, a greater understanding of phenotype polarization is still required. Moreover, better strategies and targets to induce reparative macrophagesin vivoshould guide future investigations in order to abate kidney diseases.
authors.affiliation: Experimental Nephrology, Departament de Ciències Clíniques, Universitat de Barcelona, Institut d'Investigació biomèdica de Bellvitge (IDIBELL), Hospitalet de Llobregat, Barcelona, Spain.
authors.forename: Roser
authors.initials: R
authors.lastname: Guiteras
authors.affiliation: Experimental Nephrology, Departament de Ciències Clíniques, Universitat de Barcelona, Institut d'Investigació biomèdica de Bellvitge (IDIBELL), Hospitalet de Llobregat, Barcelona, Spain.
authors.forename: Maria
authors.initials: M
authors.lastname: Flaquer
authors.affiliation: Experimental Nephrology, Departament de Ciències Clíniques, Universitat de Barcelona, Institut d'Investigació biomèdica de Bellvitge (IDIBELL), Hospitalet de Llobregat, Barcelona, Spain; Nephrology Department, Hospital Universitari de Bellvitge, Hospitalet de Llobregat, Barcelona, Spain.
authors.forename: Josep M
authors.initials: JM
authors.lastname: Cruzado
keywords: alternatively activated macrophages; end-stage renal failure; phenotype polarization; therapeutic strategy