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细胞外基质周转与流出阻力。

Extracellular matrix turnover and outflow resistance.

作者信息

Keller Kate E, Aga Mini, Bradley John M, Kelley Mary J, Acott Ted S

机构信息

Casey Eye Institute, Oregon Health and Science University, Portland, OR 97239-4197, USA.

出版信息

Exp Eye Res. 2009 Apr;88(4):676-82. doi: 10.1016/j.exer.2008.11.023. Epub 2008 Dec 6.

Abstract

Normal homeostatic adjustment of elevated intraocular pressure (IOP) involves remodeling the extracellular matrix (ECM) of the trabecular meshwork (TM). This entails sensing elevated IOP, releasing numerous activated proteinases to degrade existing ECM and concurrent biosynthesis of replacement ECM components. To increase or decrease IOP, the quantity, physical properties and/or organization of new components should be somewhat different from those replaced in order to modify outflow resistance. ECM degradation and replacement biosynthesis in the outflow pathway must be tightly controlled and focused to retain the complex structural organization of the tissue. Recently identified podosome- or invadopodia-like structures (PILS) may aid in the focal degradation of ECM and organization of replacement components.

摘要

眼内压(IOP)升高时的正常稳态调节涉及小梁网(TM)细胞外基质(ECM)的重塑。这需要感知升高的眼内压,释放多种活化蛋白酶以降解现有的细胞外基质,并同时进行替代细胞外基质成分的生物合成。为了升高或降低眼内压,新成分的数量、物理性质和/或组织应与被替代成分有所不同,以便改变流出阻力。流出途径中的细胞外基质降解和替代生物合成必须受到严格控制并集中进行,以保持组织复杂的结构组织。最近发现的足体样或侵袭性伪足样结构(PILS)可能有助于细胞外基质的局部降解和替代成分的组织。

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