Please use this identifier to cite or link to this item: https://repository.monashhealth.org/monashhealthjspui/handle/1/30973
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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