Lysyl Oxidase Like 1 (LOXL1) is a gene that encodes for the LOXL1 enzyme. This enzyme is required for elastin biogenesis and collagen cross-linking, polymerising tropoelastin monomers into elastin polymers. Its main role is in elastin homeostasis and matrix remodelling during injury, fibrosis and cancer development. Because of its vast range of biological functions, abnormalities in LOXL1 underlie many disease processes. Decreased LOXL1 expression is observed in disorders of elastin such as Cutis Laxa and increased expression is reported in fibrotic disease such as Idiopathic Pulmonary Fibrosis. LOXL1 is also downregulated in the lamina cribrosa in pseudoexfoliation glaucoma and genetic variants in the LOXL1 gene have been linked with an increased risk of developing pseudoexfoliation glaucoma and pseudoexfoliation syndrome. However the two major risk alleles are reversed in certain ethnic groups and are present in a large proportion of the normal population, implying complex genetic and environmental regulation is involved in disease pathogenesis. It also appears that the non-coding variants in intron 1 of LOXL1 may be involved in the regulation of LOXL1 expression. Gene alteration may occur via a number of epigenetic and post translational mechanisms such as DNA methylation, long non-coding RNAs and microRNAs. These may represent future therapeutic targets for disease. Environmental factors such as hypoxia, oxidative stress and ultraviolet radiation exposure alter LOXL1 expression, and it is likely a combination of these genetic and environmental factors that influence disease development and progression. In this review, we discuss LOXL1 properties, biological roles and regulation in detail with a focus on pseudoexfoliation syndrome and glaucoma.

中文翻译：

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像1的赖氨酰氧化酶：生物作用和调节。

像1的赖氨酰氧化酶（LOXL1）是编码LOXL1酶的基因。该酶是弹性蛋白生物发生和胶原蛋白交联所必需的，从而将原弹性蛋白单体聚合成弹性蛋白聚合物。它的主要作用是在损伤，纤维化和癌症发展过程中的弹性蛋白稳态和基质重塑。由于其广泛的生物学功能，LOXL1的异常是许多疾病过程的基础。在弹性蛋白如角质疏松症中观察到LOXL1表达降低，并且在纤维化疾病如特发性肺纤维化中报道表达升高。LOXL1在假性青光眼青光眼的椎板中也被下调，并且LOXL1基因的遗传变异与假性青光眼和假性青光眼综合征发展的风险增加相关。但是，这两个主要的风险等位基因在某些种族中是相反的，并存在于正常人群的很大一部分中，这意味着复杂的遗传和环境调控与疾病的发病机理有关。还似乎LOXL1的内含子1中的非编码变体可能参与了LOXL1表达的调节。基因改变可能通过许多表观遗传和翻译后机制发生，例如DNA甲基化，长的非编码RNA和microRNA。这些可能代表了疾病的未来治疗目标。诸如缺氧，氧化应激和紫外线照射等环境因素会改变LOXL1的表达，很可能是这些遗传和环境因素共同影响了疾病的发展和进程。在这篇评论中，我们讨论LOXL1属性，