Inflammation is a central element of many neurodegenerative diseases. Formyl peptide receptors (FPRs) can trigger several receptor-dependent signal transduction pathways that play a key role in neuroinflammation and neurodegeneration. They are chemotactic receptors that help to regulate pro- and anti-inflammatory responses in most mammals. FPRs are primarily expressed in the immune and nervous systems where they interact with a complex pattern of pathogen-derived and host-endogenous molecules. Mounting evidence points towards a contribution of FPRs – via neuropathological ligands such as Amyloid beta, and neuroprotective ligands such as Humanin, Lipoxin A4, and Annexin A1 – to multiple pathological aspects of neurodegenerative diseases. In this review, we aim to summarize the interplay of FPRs with neuropathological and neuroprotective ligands. Next, we depict their capability to trigger a number of ligand-dependent cell signaling pathways and their potential to interact with additional intracellular cofactors. Moreover, we highlight first studies, demonstrating that a pharmacological inhibition of FPRs helps to ameliorate neuroinflammation, which may pave the way towards novel therapeutic strategies.

中文翻译：

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甲酰肽受体对神经退行性疾病的新贡献

炎症是许多神经退行性疾病的核心要素。甲酰肽受体 (FPR) 可以触发几种受体依赖性信号转导通路，这些通路在神经炎症和神经退行性变中起关键作用。它们是趋化受体，有助于调节大多数哺乳动物的促炎和抗炎反应。FPR 主要在免疫和神经系统中表达，它们与病原体衍生和宿主内源性分子的复杂模式相互作用。越来越多的证据表明 FPR 对神经退行性疾病的多个病理方面的贡献——通过诸如淀粉样蛋白 β 之类的神经病理学配体和诸如 Humanin、脂氧素 A4 和膜联蛋白 A1 之类的神经保护性配体。在这篇综述中，我们旨在总结 FPR 与神经病理学和神经保护配体的相互作用。接下来，我们描述了它们触发许多配体依赖性细胞信号通路的能力以及它们与其他细胞内辅助因子相互作用的潜力。此外，我们强调了第一项研究，证明 FPR 的药理学抑制有助于改善神经炎症，这可能为新的治疗策略铺平道路。