Microglia and inflammation: conspiracy, controversy or control?

被引:156
作者
Fernandes, Adelaide [1 ,2 ]
Miller-Fleming, Leonor [3 ]
Pais, Teresa F. [3 ]
机构
[1] Univ Lisbon, Fac Farm, Res Inst Med iMed ULisboa, P-1649003 Lisbon, Portugal
[2] Univ Lisbon, Dept Biochem & Human Biol, Fac Farm, P-1649003 Lisbon, Portugal
[3] Inst Med Mol, P-1649028 Lisbon, Portugal
关键词
Central nervous system; Therapies; Neurologic diseases; NF-KAPPA-B; CENTRAL-NERVOUS-SYSTEM; VASOACTIVE-INTESTINAL-PEPTIDE; ACTIVATING POLYPEPTIDE INHIBIT; MULTIPLE-SCLEROSIS LESIONS; DEPENDENT GENE-EXPRESSION; TOLL-LIKE RECEPTOR; ALZHEIMERS-DISEASE; NITRIC-OXIDE; MOUSE MODEL;
D O I
10.1007/s00018-014-1670-8
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Microglial cells contribute to normal function of the central nervous system (CNS). Besides playing a role in the innate immunity, they are also involved in neuronal plasticity and homeostasis of the CNS. While microglial cells get activated and undergo phenotypic changes in different disease contexts, they are far from being the "villains" in the CNS. Mounting evidence indicates that microglial dysfunction can exacerbate the pathogenesis of several diseases in the CNS. Several molecular mechanisms tightly regulate the production of inflammatory and toxic factors released by microglia. These mechanisms involve the interaction with other glial cells and neurons and the fine regulation of signaling and transcription activation pathways. The purpose of this review is to discuss microglia activation and to highlight the molecular pathways that can counteract the detrimental role of microglia in several neurologic diseases. Recent work presented in this review support that the understanding of microglial responses can pave the way to design new therapies for inflammatory diseases of the CNS.
引用
收藏
页码:3969 / 3985
页数:17
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