Retinal remodeling.
Retinal remodeling.
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DOI：
10.1007/s10384-012-0147-2
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发表时间：
2012-07
影响因子：
2.4
通讯作者：
Marc, R. E.
中科院分区：
文献类型：
--
作者：
Jones, B. W.;Kondo, M.;Terasaki, H.;Lin, Y.;McCall, M.;Marc, R. E.
视网膜光感受器变性有多种形式。视紫红质基因突变或视网膜色素上皮疾病、三磷酸腺苷结合盒转运蛋白缺陷、ABCR基因缺陷、受体酪氨酸激酶缺陷、纤毛病和转运缺陷、转导素和抑制蛋白缺陷、视杆环鸟苷3′，5 ′-磷酸磷酸二酯酶缺陷、外周蛋白缺陷、代谢型谷氨酸受体缺陷、合成酶缺陷、与信号传导相关的基因缺陷，以及更多的缺陷都可能导致视网膜变性疾病，如视网膜色素变性（RP）或RP样疾病。视网膜相关性黄斑变性（AMD）和AMD样疾病可能是由于潜在的基因靶点和基因/基因相互作用的星座，而其他缺陷导致糖尿病视网膜病变或青光眼。然而，所有这些损伤以及对视网膜的创伤性损伤导致视网膜重塑。视网膜重塑是视网膜变性疾病之后的普遍发现，其导致神经视网膜从光感受器输入的去传入，因为下游神经元元件以负可塑性响应输入的损失。这种负可塑性在光感受器变性面前不是被动的，在分子、突触、细胞和组织水平上发现视网膜结构和功能的阶段性修正，涉及视网膜中的所有细胞类别，包括神经元和神经胶质。视网膜重塑对通过仿生或生物方法挽救视力丧失具有直接影响，因为视网膜中的回路修正破坏了对残余神经视网膜的任何潜在替代感光器输入。然而，通过对视网膜重塑的研究揭示了许多潜在的干预机会，包括旨在减缓感光细胞丧失的治疗，旨在限制或阻止重塑事件的干预措施，以及靶向残余神经视网膜中适当类别的神经元的个体发育方法。
Retinal photoreceptor degeneration takes many forms. Mutations in rhodopsin genes or disorders of the retinal pigment epithelium, defects in the adenosine triphosphate binding cassette transporter, ABCR gene defects, receptor tyrosine kinase defects, ciliopathies and transport defects, defects in both transducin and arrestin, defects in rod cyclic guanosine 3′,5′-monophosphate phosphodiesterase, peripherin defects, defects in metabotropic glutamate receptors, synthetic enzymatic defects, defects in genes associated with signaling, and many more can all result in retinal degenerative disease like retinitis pigmentosa (RP) or RP-like disorders. Age-related macular degeneration (AMD) and AMD-like disorders are possibly due to a constellation of potential gene targets and gene/gene interactions, while other defects result in diabetic retinopathy or glaucoma. However, all of these insults as well as traumatic insults to the retina result in retinal remodeling. Retinal remodeling is a universal finding subsequent to retinal degenerative disease that results in deafferentation of the neural retina from photoreceptor input as downstream neuronal elements respond to loss of input with negative plasticity. This negative plasticity is not passive in the face of photoreceptor degeneration, with a phased revision of retinal structure and function found at the molecular, synaptic, cell, and tissue levels involving all cell classes in the retina, including neurons and glia. Retinal remodeling has direct implications for the rescue of vision loss through bionic or biological approaches, as circuit revision in the retina corrupts any potential surrogate photoreceptor input to a remnant neural retina. However, there are a number of potential opportunities for intervention that are revealed through the study of retinal remodeling, including therapies that are designed to slow down photoreceptor loss, interventions that are designed to limit or arrest remodeling events, and oplogenetic approaches that target appropriate classes of neurons in the remnant neural retina.
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影响因子：
1.8
作者：
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通讯作者：
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