NATURE . COM {
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We are analyzing https://www.nature.com/articles/s41581-019-0110-2.
Title:
Macrophages: versatile players in renal inflammation and fibrosis | Nature Reviews Nephrology
Description:
Macrophages have important roles in immune surveillance and in the maintenance of kidney homeostasis; their response to renal injury varies enormously depending on the nature and duration of the insult. Macrophages can adopt a variety of phenotypes: at one extreme, M1 pro-inflammatory cells contribute to infection clearance but can also promote renal injury; at the other extreme, M2 anti-inflammatory cells have a reparative phenotype and can contribute to the resolution phase of the response to injury. In addition, bone marrow monocytes can differentiate into myeloid-derived suppressor cells that can regulate T cell immunity in the kidney. However, macrophages can also promote renal fibrosis, a major driver of progression to end-stage renal disease, and the CD206+ subset of M2 macrophages is strongly associated with renal fibrosis in both human and experimental diseases. Myofibroblasts are important contributors to renal fibrosis and recent studies provide evidence that macrophages recruited from the bone marrow can transition directly into myofibroblasts within the injured kidney. This process is termed macrophage-to-myofibroblast transition (MMT) and is driven by transforming growth factor-β1 (TGFβ1)–Smad3 signalling via a Src-centric regulatory network. MMT may serve as a key checkpoint for the progression of chronic inflammation into pathogenic fibrosis. Macrophages are versatile immune cells that protect the host against infection but can also promote chronic inflammation and fibrosis. In this Review, the authors discuss the diverse roles of macrophages in acute and chronic renal pathology as well as potential therapeutic targets.
Website Age:
30 years and 10 months (reg. 1994-08-11).
Title:
Macrophages: versatile players in renal inflammation and fibrosis | Nature Reviews Nephrology
Description:
Macrophages have important roles in immune surveillance and in the maintenance of kidney homeostasis; their response to renal injury varies enormously depending on the nature and duration of the insult. Macrophages can adopt a variety of phenotypes: at one extreme, M1 pro-inflammatory cells contribute to infection clearance but can also promote renal injury; at the other extreme, M2 anti-inflammatory cells have a reparative phenotype and can contribute to the resolution phase of the response to injury. In addition, bone marrow monocytes can differentiate into myeloid-derived suppressor cells that can regulate T cell immunity in the kidney. However, macrophages can also promote renal fibrosis, a major driver of progression to end-stage renal disease, and the CD206+ subset of M2 macrophages is strongly associated with renal fibrosis in both human and experimental diseases. Myofibroblasts are important contributors to renal fibrosis and recent studies provide evidence that macrophages recruited from the bone marrow can transition directly into myofibroblasts within the injured kidney. This process is termed macrophage-to-myofibroblast transition (MMT) and is driven by transforming growth factor-β1 (TGFβ1)–Smad3 signalling via a Src-centric regulatory network. MMT may serve as a key checkpoint for the progression of chronic inflammation into pathogenic fibrosis. Macrophages are versatile immune cells that protect the host against infection but can also promote chronic inflammation and fibrosis. In this Review, the authors discuss the diverse roles of macrophages in acute and chronic renal pathology as well as potential therapeutic targets.
Website Age:
30 years and 10 months (reg. 1994-08-11).
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Keywords {🔍}
pubmed, google, scholar, cas, renal, kidney, central, fibrosis, macrophage, nephrol, macrophages, injury, cells, int, disease, soc, glomerulonephritis, nature, phenotype, cell, human, diabetic, role, nephropathy, inflammation, nikolicpaterson, physiol, mice, bone, chronic, activation, kinase, signaling, transplant, immunol, pathol, progression, experimental, tissue, expression, receptor, acute, interstitial, lan, repair, invest, med, factor, polarization, rat,
Topics {✒️}
nature portfolio journals permissions reprints nature portfolio privacy policy cd32b-smad3-mtor signaling pathway m-csf/c-fms pathway rebalancing tgf-beta/smad signaling platelet-derived growth factor deoxycorticosterone/salt-induced cardiac fibrosis tgf-beta1/smad3 signaling protects advertising single-cell rna-seq reveals tgf-beta/smad3 signalling regulates il-4/il-10/tgf-beta yields medical research fund medical research council transforming growth factor-β1 research grants council social media regional differences necrotic cell dna activates src-kinases-controlled cellular functions src-centric regulatory network bone marrow-derived cells macrophage-derived growth factors myeloid-derived suppressor cells virus-induced monocyte differentiation bone marrow-derived fibroblasts hui-yao lan author information authors bone marrow-derived macrophages aldosterone-independent cardiac fibrosis streptozotocin-induced diabetic glomerulopathy cisplatin-induced renal injury monocyte-derived suppressor cells experimental anti-gbm glomerulonephritis drug-induced gingival hyperplasia c-fms suppresses tgf-beta induces m2 c-reactive protein antibody-mediated glomerular injury spleen tyrosine kinase crescentic anti-gbm glomerulonephritis renal ischaemia/reperfusion injury rhabdomyolysis-induced kidney injury il-4/il-13-mediated polarization nature nature+ nature 359 macrophage-mediated renal injury
Questions {❓}
- CX3CL1/CX3CR1 axis, as the therapeutic potential in renal diseases: friend or foe?
- Diabetic nephropathy — is this an immune disorder?
Schema {🗺️}
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headline:Macrophages: versatile players in renal inflammation and fibrosis
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