Glaucomatous cupping of the lamina cribrosa: a review of the evidence for active progressive remodeling as a mechanism.
Glaucomatous cupping of the lamina cribrosa: a review of the evidence for active progressive remodeling as a mechanism.
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DOI：
10.1016/j.exer.2010.08.004
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发表时间：
2011-08
影响因子：
3.4
通讯作者：
Sigal, Ian A.
中科院分区：
文献类型：
--
作者：
Downs, J. Crawford;Roberts, Michael D.;Sigal, Ian A.
关键词：
这篇评论的目的是检查文献，试图阐明昏迷拔罐的生物力学基础。特别是，这项工作的重点是生物力学的作用，在驱动结缔组织重塑的层状形态的进展，从正常状态的挖掘hepatocomatous状态。虽然有多种因素对青光眼的发病机制，我们专注于层细胞外基质（ECM）重塑青光眼和反馈机制和信号，可能会引导渐进层杯。我们回顾了在神经性昏迷的发病和进展的生物力学范例的背景下，在解剖，结构，细胞和亚细胞水平的层状ECM神经性昏迷的变化的潜在机制的文献。从这次审查中可以得出几个结论。首先，原发性开角型青光眼中筛板ECM发生广泛重塑。第二，很少有证据支持急性机械损伤椎板的主要机制，杯。第三，ONH星形胶质细胞和筛板细胞可以感受到它们的机械环境，并通过重塑ECM对机械刺激作出反应。第四，有证据表明椎板的慢性重塑导致椎板插入管壁的进行性后移，最终导致后椎板插入软脑膜。最后，建模研究表明，层流重塑可能是一种生物力学反馈机制，通过该机制，细胞改变其环境，试图返回到稳态的机械环境。生物力学驱动的结缔组织重塑是层流形态从正常状态发展到杯状、凹陷性昏迷状态的一种机制，这是合理的。
The purpose of this review is to examine the literature in an attempt to elucidate a biomechanical basis for glaucomatous cupping. In particular, this work focuses on the role of biomechanics in driving connective tissue remodeling in the progression of laminar morphology from a normal state to that of an excavated glaucomatous state. While there are multiple contributing factors to the pathogenesis of glaucoma, we focus on laminar extracellular matrix (ECM) remodeling in glaucoma and the feedback mechanisms and signals that may guide progressive laminar cupping. We review the literature on the potential mechanisms of glaucomatous changes in the laminar ECM at the anatomic, structural, cellular and subcellular levels in the context of the biomechanical paradigm of glaucomatous onset and progression. From this review several conclusions can be drawn. First, extensive remodeling of the lamina cribrosa ECM occurs in primary open angle glaucoma. Second, there is surprisingly little evidence to support acute mechanical damage to the lamina as the principal mechanism of cupping. Third, ONH astrocytes and lamina cribrosa cells can sense their mechanical environment and respond to mechanical stimuli by remodeling the ECM. Fourth, there is evidence suggesting that chronic remodeling of the lamina results in a progressive posterior migration of the laminar insertion into the canal wall, which eventually results in the posterior lamina inserting into the pia mater. Finally, modeling studies suggest that laminar remodeling may be a biomechanical feedback mechanism through which cells modify their environment in an attempt to return to a homeostatic mechanical environment. It is plausible that biomechanics-driven connective tissue remodeling is a mechanism in the progression of laminar morphology from a normal state to that of a cupped, excavated glaucomatous state.
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影响因子：
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通讯作者：
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