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光感受器细胞稳态和存活的新兴溶酶体功能。

Emerging Lysosomal Functions for Photoreceptor Cell Homeostasis and Survival.

机构信息

Department of Biology, University of Naples Federico II, Strada Vicinale Cupa Cinthia, 26, 80126 Naples, Italy.

Telethon Institute of Genetics and Medicine, Via Campi Flegrei 34, 80078 Pozzuoli, Italy.

出版信息

Cells. 2021 Dec 26;11(1):60. doi: 10.3390/cells11010060.

DOI:10.3390/cells11010060
PMID:35011622
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8750961/
Abstract

Lysosomes are membrane-bound cell organelles that respond to nutrient changes and are implicated in cell homeostasis and clearance mechanisms, allowing effective adaptation to specific cellular needs. The relevance of the lysosome has been elucidated in a number of different contexts. Of these, the retina represents an interesting scenario to appreciate the various functions of this organelle in both physiological and pathological conditions. Growing evidence suggests a role for lysosome-related mechanisms in retinal degeneration. Abnormal lysosomal activation or inhibition has dramatic consequences on photoreceptor cell homeostasis and impacts extensive cellular function, which in turn affects vision. Based on these findings, a series of therapeutic methods targeting lysosomal processes could offer treatment for blindness conditions. Here, we review the recent findings on membrane trafficking, subcellular organization, mechanisms by which lysosome/autophagy pathway impairment affects photoreceptor cell homeostasis and the recent advances on developing efficient lysosomal-based therapies for retinal disorders.

摘要

溶酶体是一种受营养变化影响的膜结合细胞器,与细胞内稳态和清除机制有关,使其能够有效地适应特定的细胞需求。溶酶体的相关性在许多不同的情况下得到了阐明。在这些情况下,视网膜是一个有趣的场景,可以了解这个细胞器在生理和病理条件下的各种功能。越来越多的证据表明,溶酶体相关机制在视网膜变性中起作用。异常的溶酶体激活或抑制对光感受器细胞的内稳态有巨大的影响,并影响广泛的细胞功能,进而影响视力。基于这些发现,一系列针对溶酶体过程的治疗方法可能为失明提供治疗。在这里,我们回顾了最近关于膜转运、亚细胞组织、溶酶体/自噬途径损伤影响光感受器细胞内稳态的机制以及最近在开发用于治疗视网膜疾病的有效基于溶酶体的治疗方法方面的进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32d6/8750961/14c6a722dfdc/cells-11-00060-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32d6/8750961/511f085b9e28/cells-11-00060-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32d6/8750961/626f86323286/cells-11-00060-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32d6/8750961/14c6a722dfdc/cells-11-00060-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32d6/8750961/511f085b9e28/cells-11-00060-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32d6/8750961/626f86323286/cells-11-00060-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32d6/8750961/14c6a722dfdc/cells-11-00060-g003.jpg

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本文引用的文献

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Pathogenic mechanisms contributing to the vulnerability of aging human photoreceptor cells.导致衰老人类光感受器细胞易损性的致病机制。
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Metformin Enhances Autophagy and Normalizes Mitochondrial Function to Alleviate Aging-Associated Inflammation.二甲双胍增强自噬并使线粒体功能正常化,从而缓解与衰老相关的炎症。
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