Role of nitric oxide in regulating epidermal permeability barrier function.
Role of nitric oxide in regulating epidermal permeability barrier function.
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DOI：
10.1111/exd.14470
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发表时间：
2022-03
影响因子：
3.6
通讯作者：
Elias PM
中科院分区：
文献类型：
--
作者：
Man MQ;Wakefield JS;Mauro TM;Elias PM
一氧化氮 (NO) 是一种由一氧化氮合酶 (NOS) 合成的自由基分子，调节多种细胞类型的多种细胞功能。这些NOS，包括内皮型NOS (eNOS)、诱导型NOS (iNOS) 和神经型NOS (nNOS)，在角质形成细胞中表达。 iNOS 和 nNOS 的表达水平随着年龄的增长而降低，NO 不足与糖尿病和高血压等多种疾病的发生以及动脉粥样硬化的严重程度有关。相反，过量的一氧化氮水平会诱发细胞氧化应激，但维持细胞（包括角质形成细胞）的正常功能需要生理水平的一氧化氮。 NO 还通过刺激角质形成细胞增殖、分化和脂质代谢来调节皮肤功能，包括表皮通透性屏障稳态和伤口愈合。局部应用多种产生一氧化氮（称为 NO 供体）的药物，如 S-亚硝基-N-乙酰基-D,L-青霉胺 (SNAP)，可以延迟屏障破坏皮肤的渗透性屏障恢复，但表皮渗透性屏障稳态仍需要 iNOS。本综述总结了 NO 在表皮通透性屏障功能中的调节作用及其相关机制。
Nitric oxide (NO), a free radical molecule synthesized by nitric oxide synthases (NOS), regulates multiple cellular functions in a variety of cell types. These NOS, including endothelial NOS (eNOS), inducible NOS (iNOS) and neural NOS (nNOS), are expressed in keratinocytes. Expression levels of both iNOS and nNOS decrease with aging, and insufficient NO has been linked to the development of a number of disorders such as diabetes and hypertension, and to the severity of atherosclerosis. Conversely, excessive NO levels can induce cellular oxidative stress, but physiological levels of NO are required to maintain the normal functioning of cells, including keratinocytes. NO also regulates cutaneous functions, including epidermal permeability barrier homeostasis and wound healing, through its stimulation of keratinocyte proliferation, differentiation and lipid metabolism. Topical applications of a diverse group of agents which generate nitric oxide (called NO donors) such as S-nitroso-N-acetyl-D,L-penicillamine (SNAP) can delay permeability barrier recovery in barrier-disrupted skin, but iNOS is still required for epidermal permeability barrier homeostasis. This review summarizes the regulatory role that NO plays in epidermal permeability barrier functions and the underlying mechanisms involved.
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影响因子：
6
作者：
Demerjian, Marianne;Hachem, Jean-Pierre;Feingold, Kenneth R.
通讯作者：
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DOI：
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发表时间：
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DOI：
10.1073/pnas.012368499
发表时间：
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影响因子：
11.1
作者：
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通讯作者：
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