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Comment
. 2013 Jan;34(1):6-7.
doi: 10.1038/aps.2012.178. Epub 2012 Dec 24.

The good and bad of microglia/macrophages: new hope in stroke therapeutics

Ya-chi Huang  1 , Zhong-ping Feng
Affiliations
Comment

The good and bad of microglia/macrophages: new hope in stroke therapeutics

Ya-chi Huang et al. Acta Pharmacol Sin. 2013 Jan.
No abstract available

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Figures

Figure 1
Figure 1
Microglia/macrophages possess dual but opposite roles in the inflammatory responses progression in stroke. At early stage of hypoxic/anoxic condition, microglia/macrophages are mostly differentiated into the neuroprotective M2 phenotype. With time, microglia/macrophages gradually transform into a neuronal injurious M1 phenotype. M1 phenotype is “classically activated via toll-like receptors or interferon-γ”, whereas M2 phenotype is “alternatively activated by interleukin 4 or interleukin 13”. Future investigation identifying new therapeutic agents that promote macrophage differentiation into M2 phenotype and suppress transformation of macrophage into M1 phenotype would be valuable in treating post-ischemic stroke inflammation. (IL-4, interleukin 4; IL-13, interleukin 13; TLR, toll-like receptor; IFN-γ, interferon-γ)
See this image and copyright information in PMC

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