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The molecular basis of neurotrophic keratopathy: Diagnostic and therapeutic implications. A review
The Ocular Surface ( IF 5.9 ) Pub Date : 2020-10-03 , DOI: 10.1016/j.jtos.2020.09.007
Raul E Ruiz-Lozano 1 , Julio C Hernandez-Camarena 1 , Denise Loya-Garcia 1 , Jesus Merayo-Lloves 2 , Alejandro Rodriguez-Garcia 1
Affiliation  

Neurotrophic keratopathy (NK) is a degenerative corneal disease produced by different factors, including infection, trauma, and neurogenesis, that lead to trigeminal nerve damage and impaired corneal sensitivity. Extensive epithelial breakdown, impaired corneal epithelial healing and corneal ulceration, stromal melting, and perforation are main NK features. The proliferation of the corneal epithelium is endogenously regulated by a balance between adrenergic cAMP-dependent and cholinergic cGMP-dependent pathways. A careful balance of epitheliotropic neuromediators and neurotrophic factors expressed by corneal nerves and epithelial cells, respectively, is required to maintain corneal homeostasis. Even in its early stages, NK can cause reduced vision secondary to epithelial disturbance. Diagnosing NK is challenging, requiring the acquisition of a thorough clinical history and a comprehensive neurological and ophthalmic examination. Following suspicion of a clinical NK diagnosis, corneal sensitivity must be assessed qualitatively with the wisp of the cotton-tipped applicator and quantitatively through Cochet-Bonnet esthesiometry (CBE). A myriad of therapies is used for NK, and new, more specific modalities are being developed and investigated. Medical treatment with topical recombinant human nerve growth factor and surgical treatment through corneal neurotization are promising therapies aiming to target NK pathophysiology. Coexistent ocular surface disorders must be managed concomitantly to improve its prognosis. This review describes the up-to-date knowledge of the molecular basis regarding the pathogenesis of NK, and the novel target-specific therapeutic approaches based on this molecular mechanism.



中文翻译:

神经营养性角膜病变的分子基础:诊断和治疗意义。回顾

神经营养性角膜病变(NK)是一种由多种因素引起的变性性角膜疾病,包括感染,创伤和神经发生,可导致三叉神经损伤和角膜敏感性受损。NK的主要特征是广泛的上皮破裂,角膜上皮愈合受损,角膜溃疡,基质融化和穿孔。角膜上皮细胞的增殖受肾上腺素cAMP依赖性和胆碱能cGMP依赖性途径之间的平衡内源性调节。分别维持角膜神经和上皮细胞表达的上皮性神经介导因子和神经营养因子之间的谨慎平衡,才能维持角膜稳态。即使在早期,NK也会导致继发于上皮紊乱的视力下降。诊断NK具有挑战性,需要获得彻底的临床病史以及全面的神经和眼科检查。怀疑临床NK诊断后,必须用棉签涂抹器定性评估角膜敏感性,并通过Cochet-Bonnet美学测定法(CBE)定量评估。NK使用了无数种疗法,并且正在开发和研究新的,更具体的方法。用局部重组人神经生长因子进行药物治疗以及通过角膜神经化手术治疗是有希望的靶向NK病理生理学的疗法。必须同时治疗并存的眼表疾病以改善其预后。这篇综述描述了有关NK发病机理的分子基础的最新知识,

更新日期:2020-10-04
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