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Title: | Macrophage signaling pathways: A novel target in renal disease. | Authors: | Ma F.Y.;Nikolic-Paterson D.J. ;Ikezumi Y. | Institution: | (Ma, Nikolic-Paterson) Department of Nephrology and Monash University Department of Medicine, Monash Medical Centre, Clayton, VIC, Australia (Ikezumi) Department of Pediatrics, Niigata University Medical and Dental Hospital, Niigata, Japan | Issue Date: | 12-Oct-2012 | Copyright year: | 2010 | Publisher: | W.B. Saunders (Independence Square West, Philadelphia PA 19106-3399, United States) | Place of publication: | United States | Publication information: | Seminars in Nephrology. 30 (3) (pp 334-344), 2010. Date of Publication: May 2010. | Abstract: | Monocytes/macrophages are a heterogeneous cell population that play a critical role in host defense and tissue homeostasis. However, macrophage activation during acute and chronic inflammation can result in macrophage-mediated renal injury in a variety of settings, including proliferative glomerulonephritis. Macrophages can be activated via a number of intracellular signaling pathways (eg, c-Jun amino terminal kinase, p38 mitogen-activated protein kinase, FcR/Syk, Janus kinase/signal transducer and activator of transcription) that induce production of mediators of renal injury. Thus, targeting selected macrophage signaling pathways is a potential therapeutic strategy to suppress macrophage-mediated renal injury while leaving intact the desirable macrophage functions of host defense and tissue repair. © 2010 Elsevier Inc. | DOI: | http://monash.idm.oclc.org/login?url=http://dx.doi.org/10.1016/j.semnephrol.2010.03.008 | PubMed URL: | 20620676 [http://www.ncbi.nlm.nih.gov/pubmed/?term=20620676] | ISSN: | 0270-9295 | URI: | https://repository.monashhealth.org/monashhealthjspui/handle/1/30973 | Type: | Article | Subjects: | chronic inflammation cytokine production homeostasis host resistance human inflammation *kidney disease/et [Etiology] kidney injury/et [Etiology] *macrophage macrophage activation macrophage function article nonhuman priority journal proliferative glomerulonephritis/et [Etiology] signal transduction tissue repair Janus kinase/ec [Endogenous Compound] mitogen activated protein kinase p38/ec [Endogenous Compound] protein kinase Syk/ec [Endogenous Compound] STAT protein/ec [Endogenous Compound] stress activated protein kinase/ec [Endogenous Compound] monocyte macrophage activation macrophage function monocyte nonhuman priority journal proliferative glomerulonephritis / etiology signal transduction tissue repair *kidney disease / *etiology inflammation human host resistance kidney injury / etiology *macrophage homeostasis cytokine production chronic inflammation article |
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