The Fibro-Inflammatory Response in the Glaucomatous Optic Nerve Head.

The Fibro-Inflammatory Response in the Glaucomatous Optic Nerve Head.
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DOI:
10.3390/ijms241713240
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发表时间:
2023-08-26
影响因子:
5.6
通讯作者:
--
中科院分区:
生物学2区
文献类型:
--
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青光眼是一种进行性疾病,是导致不可逆失明的主要原因。有限的治疗方法只能控制青光眼的常见风险因素,即眼内压(IOP)升高,这表明非常需要了解疾病进展期间视神经乳头(ONH)损伤背后的细胞机制。在这里,我们回顾了已知的炎症和纤维化的变化发生在ONH。此外,我们描述了一种新的机制,Toll样受体4(TLR4)和转化生长因子β 2(TGFβ2)信号串扰的细胞中的ONH,有助于脑损伤。了解ONH细胞内和细胞间的分子信号传导可以帮助确定新的药物靶点和治疗方法。
Glaucoma is a progressive disease and the leading cause of irreversible blindness. The limited therapeutics available are only able to manage the common risk factor of glaucoma, elevated intraocular pressure (IOP), indicating a great need for understanding the cellular mechanisms behind optic nerve head (ONH) damage during disease progression. Here we review the known inflammatory and fibrotic changes occurring in the ONH. In addition, we describe a novel mechanism of toll-like receptor 4 (TLR4) and transforming growth factor beta-2 (TGFβ2) signaling crosstalk in the cells of the ONH that contribute to glaucomatous damage. Understanding molecular signaling within and between the cells of the ONH can help identify new drug targets and therapeutics.
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