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首页> 外文期刊>Cell Reports >NLRP3 Inflammasome Blockade Inhibits VEGF-A-Induced Age-Related Macular Degeneration
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NLRP3 Inflammasome Blockade Inhibits VEGF-A-Induced Age-Related Macular Degeneration

机译：NLRP3炎性体阻断剂抑制VEGF-A诱导的年龄相关性黄斑变性

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The NLRP3 inflammasome is activated in age-related macular degeneration (AMD), but it remains unknown whether its activation contributes to AMD pathologies. VEGF-A is increased in neovascular (''wet'') AMD, but it is not known whether it plays a role in inflammasome activation, whether an increase of VEGF-A by itself is sufficient to cause neovascular AMD and whether it can contribute to nonexudative (''dry'') AMD that often co-occurs with the neovascular form. Here, it is shown that an increase in VEGF-A results in NLRP3 inflammasome activation and is sufficient to cause both forms of AMD pathologies. Targeting NLRP3 or the inflammasome effector cytokine IL-1@b inhibits but does not prevent VEGF-A-induced AMD pathologies, whereas targeting IL-18 promotes AMD. Thus, increased VEGF-A provides a unifying pathomechanism for both forms of AMD; combining therapeutic inhibition of both VEGF-A and IL-1@b or the NLRP3 inflammasome is therefore likely to suppress both forms of AMD.
机译：NLRP3炎性小体在与年龄有关的黄斑变性（AMD）中被激活，但尚不清楚其激活是否与AMD病理有关。 VEGF-A在新生血管（“湿性”）AMD中升高，但尚不清楚它是否在炎症小体激活中起作用，VEGF-A自身升高是否足以引起新生血管性AMD，以及是否可以起到促进作用到通常与新血管形式同时出现的非渗出性（“干燥”）AMD。在这里，表明VEGF-A的增加导致NLRP3炎症小体活化，并且足以引起两种形式的AMD病理。靶向NLRP3或炎性体效应细胞因子IL-1 @ b抑制但不阻止VEGF-A诱导的AMD病变，而靶向IL-18则促进AMD。因此，增加的VEGF-A为两种形式的AMD提供了统一的发病机制。因此，将对VEGF-A和IL-1b或NLRP3炎性小体的治疗性抑制相结合可能会抑制两种形式的AMD。

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