TY - JOUR
T1 - Macrophage signaling pathways
T2 - A novel target in renal disease
AU - Ma, Frank Y.
AU - Ikezumi, Yohei
AU - Nikolic-Paterson, David J.
N1 - Funding Information:
This work was supported in part by the National Health and Medical Research Council of Australia and Ministry of Education, Culture, Sports, Science and Technology of Japan . DN-P acts as a consultant for Celgene and has received funding for studies involving JNK inhibitors as noted in individual manuscripts.
PY - 2010/5
Y1 - 2010/5
N2 - 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.
AB - 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.
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U2 - 10.1016/j.semnephrol.2010.03.008
DO - 10.1016/j.semnephrol.2010.03.008
M3 - Article
C2 - 20620676
AN - SCOPUS:77953884129
SN - 0270-9295
VL - 30
SP - 334
EP - 344
JO - Seminars in Nephrology
JF - Seminars in Nephrology
IS - 3
ER -