ArticleThe American journal of pathology2008
By homing to the kidney, activated macrophages potently exacerbate renal injury.
Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 75 citations in OpenAlex.
- Disruption of the Circadian Rhythm Induces Acute Pancreatitis via Amino Acid Metabolism-Mediated Macrophage Infiltration.Cellular and molecular gastroenterology and hepatology · 2026Article
- CCL5 paradoxically regulates glomerular injury by skewing macrophage polarization.JCI insight · 2025Article
- Relationship between complement and macrophage markers with kidney survival in patients with diabetic nephropathy.Acta diabetologica · 2025Article
- M2 macrophage infusion ameliorates diabetic glomerulopathyRenal failure · 2024Article
- Macrophage based drug delivery: Key challenges and strategies.Bioactive materials · 2024Review
- Infiltrating macrophages and interferon gamma rather than renal genotype dictate heightened crescentic glomerulonephritis.Frontiers in immunology · 2024Article
- Combination therapy with DHA and BMSCs suppressed podocyte injury and attenuated renal fibrosis by modulating the TGF-Renal failure · 2023Article
- Kidney organoid systems for studies of immune-mediated kidney diseases: challenges and opportunities.Cell and tissue research · 2021Review
- Mesenchymal Stem Cell Transplantation for the Treatment of Cognitive Frailty.The journal of nutrition, health & aging · 2021Review
- Depletion of Toll-Like Receptor-9 Attenuates Renal Tubulointerstitial Fibrosis After Ischemia-Reperfusion Injury.Frontiers in cell and developmental biology · 2021Article
- A Novel Hybrid Cytokine IL233 Mediates regeneration following Doxorubicin-Induced Nephrotoxic Injury.Scientific reports · 2019Article
- Macrophage phenotype and its relationship with renal function in human diabetic nephropathy.PloS one · 2019Article
- Nephropathy in Hypertensive Animals Is Linked to M2 Macrophages and Increased Expression of the YM1/Chi3l3 Protein.Mediators of inflammation · 2019Article
- Tubulointerstitial Infiltration of M2 Macrophages in Henoch-Schönlein Purpura Nephritis Indicates the Presence of Glomerular Crescents and Bad Clinical Parameters.BioMed research international · 2019Article
- A Noninvasive Imaging Toolbox Indicates Limited Therapeutic Potential of Conditionally Activated Macrophages in a Mouse Model of Multiple Organ Dysfunction.Stem cells international · 2019Article
- Infiltrating macrophages in diabetic nephropathy promote podocytes apoptosis via TNF-α-ROS-p38MAPK pathway.Oncotarget · 2017Article
- Broad Infiltration of Macrophages Leads to a Proinflammatory State in Streptozotocin-Induced Hyperglycemic Mice.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Dendritic Cells and Macrophages: Sentinels in the Kidney.Clinical journal of the American Society of Nephrology : CJASN · 2015Review
- CXCL10 induces the recruitment of monocyte-derived macrophages into kidney, which aggravate puromycin aminonucleoside nephrosis.Clinical and experimental immunology · 2015Article
- Artemisinin analogue SM934 ameliorates the proteinuria and renal fibrosis in rat experimental membranous nephropathy.Acta pharmacologica Sinica · 2015Article
Corrections and comments
- Erratum issuedCai, Qi [corrected to Cao, Qi]
Authors and funding
10 authors at 1 institution in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophages are important mediators of injury in most types of human kidney diseases; however, the pathogenic importance of both macrophage number and activation status is unknown. To examine this question, severe-combined immunodeficient mice with adriamycin nephrosis, an experimental model of human focal segmental glomerulosclerosis, were treated intravenously with either resting (1 x 10(6) to 5 x 10(6)) or activated (1 x 10(3) to 1 x 10(6)) macrophages on day 6 postadriamycin administration, and the effects on kidney injury were examined. On day 28, renal injury was worse in the group that received activated macrophages at doses as low as 1 x 10(4) macrophages per mouse compared with control adriamycin nephrotic mice. However, treatment with resting macrophages at doses as high as 5 x 10(6) macrophages per mouse had no significant effect on either renal histology or function. The transferred activated macrophages homed to inflamed kidneys during the middle-to-late stages of the disease, but such homing was not observed for resting macrophages. This study of in vivo cell adoptive transfer supports the importance of macrophage activation status over macrophage number in causing renal injury. These data suggest that therapeutic strategies for treating progressive kidney diseases should target activated macrophages.
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