Macrophage in chronic kidney disease

Guiteras, Roser; Flaquer, Maria; Cruzado, Josep M.

doi:10.1093/ckj/sfw096

Cited by 93 publications

(100 citation statements)

References 85 publications

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“…They can be polarized under various stimuli; subsequently, they are subdivided into distinct populations, namely proinflammatory macrophages (M1) or anti‐inflammatory macrophages (M2) (27). The M1/M2 macrophage balance is highly related to the renal microenvironment and can significantly influence chronic kidney disease progression (28).…”

Section: Resultsmentioning

confidence: 99%

NLRC5 deficiency ameliorates diabetic nephropathy through alleviating inflammation

et al. 2018

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NOD-like receptor family caspase recruitment domain family domain containing 5 (NLRC5) has important roles in inflammation and innate immunity. NLRC5 was highly expressed in kidney from streptozotocin-induced diabetic mice, db/ db mice and patients with diabetes. Based on that evidence, the present study was designed to explore the roles of NLRC5 in the progression of diabetic nephropathy (DN). We examined kidney injury, including inflammation and fibrosis in Nlrc5 gene knockout ( Nlrc5) and wild-type (WT) diabetic mice. We found that Nlrc5 mice developed less-severe diabetic kidney injury compared with WT mice, exhibiting lower albuminuria, less fibronectin and collagen IV expression, and reduced macrophage infiltration but greater levels of podocin and nephrin in the diabetic kidney. The underlying mechanisms were further investigated in vitro with peritoneal macrophages and mesangial cells treated with high glucose. Reduced proinflammatory effect was observed in peritoneal macrophages from Nlrc5 mice, associated with NF-κB pathway suppression. Knocking down of NLRC5 in mesangial cells in high-glucose conditions was also associated with reduced NF-κB and TGF-β/Smad signaling. Taken together, NLRC5 promotes inflammation and fibrosis during DN progression partly through the effects on NF-κB and TGF-β/Smad pathways. NLRC5 may, therefore, be a promising therapeutic target for DN treatment.-Luan, P., Zhuang, J., Zou, J., Li, H., Shuai, P., Xu, X., Zhao, Y., Kou, W., Ji, S., Peng, A., Xu, Y., Su, Q., Jian, W., Peng, W. NLRC5 deficiency ameliorates diabetic nephropathy through alleviating inflammation.

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Section: Resultsmentioning

confidence: 99%

NLRC5 deficiency ameliorates diabetic nephropathy through alleviating inflammation

et al. 2018

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“…Hence, modulating macrophages to a protective phenotype to reduce kidney injury in chronic kidney disease still needs further investigation. Nevertheless, the mechanisms regulating the distinct functions of macrophages during tissue repair remain largely unclear …”

Section: Introductionmentioning

confidence: 99%

“…Nevertheless, the mechanisms regulating the distinct functions of macrophages during tissue repair remain largely unclear. 21 We have previously demonstrated that anti-inflammatory effects induced by hepatocyte growth factor (HGF) gene therapy enhanced the presence of bone marrow-derived M2 (BM-ΦM2) macrophages in the glomeruli of diabetic mice and halted DKD progression. Therefore, in this study we sought to investigate whether infusion of modulated ex-vivo BM-ΦM2 macrophages provide a therapeutic effect on DKD in obese db/db mice.…”

mentioning

confidence: 99%

Exploring macrophage cell therapy on Diabetic Kidney Disease

Guiteras

Solà

Flaquer

et al. 2018

J Cellular Molecular Medi

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Alternatively activated macrophages (M2) have regenerative properties and shown promise as cell therapy in chronic kidney disease. However, M2 plasticity is one of the major hurdles to overcome. Our previous studies showed that genetically modified macrophages stabilized by neutrophil gelatinase‐associated lipocalin (NGAL) were able to preserve their M2 phenotype. Nowadays, little is known about M2 macrophage effects in diabetic kidney disease (DKD). The aim of the study was to investigate the therapeutic effect of both bone marrow‐derived M2 (BM‐фM2) and ф‐NGAL macrophages in the db/db mice. Seventeen‐week‐old mice with established DKD were divided into five treatment groups with their controls: D+BM‐фM2; D+ф‐BM; D+ф‐NGAL; D+ф‐RAW; D+SHAM and non‐diabetic (ND) (db/‐ and C57bl/6J) animals. We infused 1 × 106 macrophages twice, at baseline and 2 weeks thereafter. BM‐фM2 did not show any therapeutic effect whereas ф‐NGAL significantly reduced albuminuria and renal fibrosis. The ф‐NGAL therapy increased the anti‐inflammatory IL‐10 and reduced some pro‐inflammatory cytokines, reduced the proportion of M1 glomerular macrophages and podocyte loss and was associated with a significant decrease of renal TGF‐β1. Overall, our study provides evidence that ф‐NGAL macrophage cell therapy has a therapeutic effect on DKD probably by modulation of the renal inflammatory response caused by the diabetic milieu.

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“…A beneficial effect of M2‐macrophages has been shown in models of acute kidney injury, although their role in chronic kidney diseases is more uncertain (Guiteras et al . ).…”

Section: Discussionmentioning

confidence: 97%

“…This is of pathophysiological relevance as M2-macrophages express scavenging receptors and produce various anti-inflammatory mediators that promote the resolution of inflammation and tissue repair (Murray 2017). A beneficial effect of M2-macrophages has been shown in models of acute kidney injury, although their role in chronic kidney diseases is more uncertain (Guiteras et al 2016).…”

Section: Figurementioning

confidence: 99%