Glaucoma is a blinding diseases in which damage to the axons results in loss of retinal ganglion cells. Experimental evidence indicates that chronic intraocular pressure elevation initiates axonal insult at the level of the lamina cribrosa. The lamina cribrosa is a porous collagen structure through which the axons pass on their path from the retina to the brain. Recent experimental studies revealed the extensive structural changes of the lamina cribrosa and its surrounding tissues during the development and progression of glaucoma. In this perspective paper we review the experimental evidence for growth and remodeling mechanisms in glaucoma including adaptation of tissue anisotropy, tissue thickening/thinning, tissue elongation/shortening and tissue migration. We discuss the existing predictive computational approaches that try to elucidate the potential biomechanical basis of theses growth and remodeling mechanisms and highlight open questions, challenges, and avenues for further development.

中文翻译：

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青光眼生物力学生长和重塑机制的展望

青光眼是一种致盲疾病，其中轴突受损导致视网膜神经节细胞丢失。实验证据表明，慢性眼内压升高在筛板水平引发轴突损伤。筛板是一种多孔的胶原结构，轴突通过它从视网膜到大脑的路径上传递。最近的实验研究揭示了在青光眼的发展和进展过程中筛板及其周围组织的广泛结构变化。在这篇透视论文中，我们回顾了青光眼生长和重塑机制的实验证据，包括组织各向异性的适应、组织增厚/变薄、组织伸长/缩短和组织迁移。