Inflammatory Ocular Diseases and Sphingolipid Signaling.

Inflammatory Ocular Diseases and Sphingolipid Signaling.
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DOI:
10.1007/978-3-030-21162-2_8
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发表时间:
2019
影响因子:
--
通讯作者:
Mandal N
Mandal N
中科院分区:
医学4区
文献类型:
--
作者:
Grambergs R;Mondal K;Mandal N

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炎症是对抗组织损伤和感染的一种强有力的免疫措施。炎症反应是复杂的,需要参与无数的信号通路和代谢过程,所有这些都由众多的调节系统控制。尽管炎症是抵御组织损伤的重要防御手段,也是组织愈合的必要步骤,但即使在缺乏适当刺激的情况下,调节这种先天免疫反应的启动、强度和持续时间的机制也可能发生故障,导致不适当或失控的炎症。虽然人眼存在于免疫特权微环境中,但它也不能幸免。眼睛既不是缺乏免疫细胞,也不是完全隔绝于全身免疫反应之外,因此完全有能力通过局部炎症功能障碍和全身炎症性疾病来破坏自己(Taylor AW, Front Immunol 7:37, 2016; Zhou R, Caspi RR, Biol Rep 2, 2010)。事实上,存在多种眼部炎症性疾病,它们是人类失明的主要原因。随着对炎症过程认识的不断深入,揭示了参与炎症机制的新的关键途径和分子因子。脂质和鞘脂在眼部炎症性疾病的病理生理中具有重要的信号作用。以下是对基本炎症过程的讨论,鞘脂作为上述过程介质的地位,主要炎性眼部疾病的简要描述,以及鞘脂在其发病机制中的新发现。
Inflammation is a powerful immune counter-measure to tissue damage and infection. The inflammatory response is complex and requires the involvement of myriad signaling pathways and metabolic processes, all governed by a multitude of regulatory systems. Although inflammation is a vital defense against tissue injury and a necessary step in tissue healing, the mechanisms which modulate the initiation, intensity, and duration of this innate immune response can malfunction and result in inappropriate or out-of-control inflammation, even in the absence of an appropriate stimulus. Though the human eye exists in an immune-privileged microenvironment, it is not spared from this. The eye is neither devoid of immune cells nor is it fully sequestered from systemic immune responses, and is therefore fully capable of ruining itself through localized inflammatory dysfunction and systemic inflammatory disease (Taylor AW, Front Immunol 7:37, 2016; Zhou R, Caspi RR, Biol Rep 2, 2010). In fact, a wide range of ocular inflammatory diseases exist and are major causes of blindness in humans. Advances in the understanding of inflammatory processes have revealed new key pathways and molecular factors involved in the mechanisms of inflammation. Lipids and sphingolipids are increasingly being recognized as having important signaling roles in the pathophysiology of ocular inflammatory diseases. What follows below is a discussion of fundamental inflammatory processes, the place of sphingolipids as mediators of said processes, brief descriptions of major inflammatory ocular diseases, and new findings implicating sphingolipids in their pathogenesis.
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