• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

SSBP1 相关性视神经萎缩与黄斑病变的特征。

Characterization of SSBP1-related optic atrophy and foveopathy.

机构信息

National reference centre for inherited sensory diseases, University Hospital of Montpellier, University of Montpellier, Montpellier, France.

Sensgene Care Network, Strasbourg, France.

出版信息

Sci Rep. 2021 Sep 21;11(1):18703. doi: 10.1038/s41598-021-98150-1.

DOI:10.1038/s41598-021-98150-1
PMID:34548540
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8455542/
Abstract

Dominant optic atrophy (DOA) is genetically heterogeneous and most commonly caused by mutations in OPA1. To distinguish between the classical OPA1-related and the recently identified SSBP1-related DOAs, the retina and fovea of 27 patients carrying the SSBP1 p.Arg38Gln variant were scrutinized using 20° × 20° macular cube and 30° and 55° field fundus autofluorescence photographs. Age of onset, visual acuity, retinal nerve fiber layer and macular thicknesses were recorded. Three SSBP1-patients were asymptomatic, 10 had isolated DOA, and 12 had a combined DOA plus foveopathy. The foveopathy, with a tiny defect of the ellipsoid and interdigitation lines, was similar in all patients, independent of age. There were no significant statistical differences in terms of visual acuity and SD-OCT measurements between patients with isolated DOA (mean visual acuity in decimals: 0.54 ± 0.41) and those with combined foveopathy (0.50 ± 0.23). Two patients over 50 years of age developed a progressive rod-cone dystrophy, leading to severe visual impairment. SSBP1-related DOA shares similarities with OPA1-related DOA with an incomplete penetrance and an early childhood visual impairment. Nevertheless, the presence of a congenital foveopathy with no impact on visual acuity is a major criterion to distinguish SSBP1 cases and orient the appropriate genetic analysis.

摘要

显性视神经萎缩(DOA)具有遗传异质性,最常见的原因是 OPA1 突变。为了区分经典的 OPA1 相关 DOA 和最近发现的 SSBP1 相关 DOA,对携带 SSBP1 p.Arg38Gln 变异的 27 名患者的视网膜和黄斑进行了 20°×20° 黄斑立方和 30° 和 55° 视野眼底自发荧光照片检查。记录发病年龄、视力、视网膜神经纤维层和黄斑厚度。3 名 SSBP1 患者无症状,10 名孤立性 DOA,12 名合并 DOA 加黄斑病变。所有患者的黄斑病变均具有小的椭圆体和交织线缺陷,与年龄无关。孤立性 DOA 患者(十进制平均视力:0.54±0.41)和合并性黄斑病变患者(0.50±0.23)之间的视力和 SD-OCT 测量值没有显著统计学差异。两名 50 岁以上的患者出现进行性视杆-视锥细胞营养不良,导致严重视力损害。SSBP1 相关 DOA 与 OPA1 相关 DOA 具有相似性,表现为不完全外显率和儿童早期视力损害。然而,存在先天性黄斑病变而不影响视力是区分 SSBP1 病例并指导适当的基因分析的主要标准。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2c/8455542/752e90d47d03/41598_2021_98150_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2c/8455542/b5549e2e65fa/41598_2021_98150_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2c/8455542/ab0f8b97bd69/41598_2021_98150_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2c/8455542/42bdd636681f/41598_2021_98150_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2c/8455542/f33ef9d7a04d/41598_2021_98150_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2c/8455542/5400cc724ea0/41598_2021_98150_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2c/8455542/752e90d47d03/41598_2021_98150_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2c/8455542/b5549e2e65fa/41598_2021_98150_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2c/8455542/ab0f8b97bd69/41598_2021_98150_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2c/8455542/42bdd636681f/41598_2021_98150_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2c/8455542/f33ef9d7a04d/41598_2021_98150_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2c/8455542/5400cc724ea0/41598_2021_98150_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb2c/8455542/752e90d47d03/41598_2021_98150_Fig6_HTML.jpg

相似文献

1
Characterization of SSBP1-related optic atrophy and foveopathy.SSBP1 相关性视神经萎缩与黄斑病变的特征。
Sci Rep. 2021 Sep 21;11(1):18703. doi: 10.1038/s41598-021-98150-1.
2
The importance of genome sequencing: unraveling variant missed by exome sequencing.基因组测序的重要性:揭示外显子组测序遗漏的变异。
Ophthalmic Genet. 2023 Jun;44(3):286-290. doi: 10.1080/13816810.2022.2109685. Epub 2022 Aug 10.
3
Dominant mutations in mtDNA maintenance gene SSBP1 cause optic atrophy and foveopathy.mtDNA 维持基因 SSBP1 的显性突变导致视神经萎缩和黄斑病变。
J Clin Invest. 2020 Jan 2;130(1):143-156. doi: 10.1172/JCI128513.
4
SSBP1 mutations in dominant optic atrophy with variable retinal degeneration.SSBP1 突变导致的显性视神经萎缩伴视网膜变性的可变表现型。
Ann Neurol. 2019 Sep;86(3):368-383. doi: 10.1002/ana.25550. Epub 2019 Jul 31.
5
SSBP1-Disease Update: Expanding the Genetic and Clinical Spectrum, Reporting Variable Penetrance and Confirming Recessive Inheritance.SSBP1 病征更新:扩大遗传和临床谱,报告可变外显率并证实隐性遗传。
Invest Ophthalmol Vis Sci. 2021 Dec 1;62(15):12. doi: 10.1167/iovs.62.15.12.
6
Dominant optic atrophy.优势侧视神经萎缩。
Orphanet J Rare Dis. 2012 Jul 9;7:46. doi: 10.1186/1750-1172-7-46.
7
SSBP1 faux pas in mitonuclear tango causes optic neuropathy.SSBP1 差池导致的线粒体-核相互作用性视神经病变。
J Clin Invest. 2020 Jan 2;130(1):62-64. doi: 10.1172/JCI132532.
8
SSBP1 mutations cause mtDNA depletion underlying a complex optic atrophy disorder.SSBP1 突变导致 mtDNA 耗竭,是一种复杂的视神经萎缩疾病的基础。
J Clin Invest. 2020 Jan 2;130(1):108-125. doi: 10.1172/JCI128514.
9
Optical Coherence Tomography of the Retinal Ganglion Cell Complex in Leber's Hereditary Optic Neuropathy and Dominant Optic Atrophy.Leber 遗传性视神经病变和显性视神经萎缩的视网膜神经节细胞复合体的光相干断层扫描。
Curr Eye Res. 2019 Jun;44(6):638-644. doi: 10.1080/02713683.2019.1567792. Epub 2019 Feb 4.
10
Early-onset severe neuromuscular phenotype associated with compound heterozygosity for OPA1 mutations.早发型严重神经肌肉表型与 OPA1 突变的复合杂合性相关。
Mol Genet Metab. 2011 Aug;103(4):383-7. doi: 10.1016/j.ymgme.2011.04.018. Epub 2011 May 7.

引用本文的文献

1
A case with bilateral C-shaped autofluorescence in retinal degeneration.一例视网膜变性伴双侧C形自发荧光的病例。
Am J Ophthalmol Case Rep. 2025 May 2;38:102351. doi: 10.1016/j.ajoc.2025.102351. eCollection 2025 Jun.
2
Mitochondria in Retinal Ganglion Cells: Unraveling the Metabolic Nexus and Oxidative Stress.视网膜神经节细胞中的线粒体:揭开代谢关联和氧化应激之谜。
Int J Mol Sci. 2024 Aug 7;25(16):8626. doi: 10.3390/ijms25168626.
3
Structures of the mitochondrial single-stranded DNA binding protein with DNA and DNA polymerase γ.

本文引用的文献

1
Progression of Retinopathy Secondary to Maternally Inherited Diabetes and Deafness - Evaluation of Predicting Parameters.由母系遗传性糖尿病和耳聋引发的视网膜病变的进展-预测参数的评估。
Am J Ophthalmol. 2020 May;213:134-144. doi: 10.1016/j.ajo.2020.01.013. Epub 2020 Jan 24.
2
SSBP1 faux pas in mitonuclear tango causes optic neuropathy.SSBP1 差池导致的线粒体-核相互作用性视神经病变。
J Clin Invest. 2020 Jan 2;130(1):62-64. doi: 10.1172/JCI132532.
3
SSBP1 mutations cause mtDNA depletion underlying a complex optic atrophy disorder.
线粒体单链 DNA 结合蛋白与 DNA 和 DNA 聚合酶 γ 的结构。
Nucleic Acids Res. 2024 Sep 23;52(17):10329-10340. doi: 10.1093/nar/gkae670.
4
Maternal mosaicism in SSBP1 causing optic atrophy with retinal degeneration: implications for genetic counseling.SSBP1 所致视神经萎缩伴视网膜变性的母源性嵌合体:遗传咨询的意义。
Orphanet J Rare Dis. 2023 May 31;18(1):131. doi: 10.1186/s13023-023-02748-9.
5
Maternal Mosaicism in SSBP1 Causing Optic Atrophy with Retinal Degeneration: Implications for Genetic Counseling.SSBP1基因的母体镶嵌现象导致视神经萎缩伴视网膜变性:对遗传咨询的启示
Res Sq. 2023 Mar 15:rs.3.rs-2554402. doi: 10.21203/rs.3.rs-2554402/v1.
6
Photoreceptor Manifestations of Primary Mitochondrial Optic Nerve Disorders.原发性线粒体视神经病变的光感受器表现。
Invest Ophthalmol Vis Sci. 2022 May 2;63(5):5. doi: 10.1167/iovs.63.5.5.
7
Mitochondrial Neurodegeneration.线粒体神经退行性变。
Cells. 2022 Feb 11;11(4):637. doi: 10.3390/cells11040637.
SSBP1 突变导致 mtDNA 耗竭,是一种复杂的视神经萎缩疾病的基础。
J Clin Invest. 2020 Jan 2;130(1):108-125. doi: 10.1172/JCI128514.
4
Dominant mutations in mtDNA maintenance gene SSBP1 cause optic atrophy and foveopathy.mtDNA 维持基因 SSBP1 的显性突变导致视神经萎缩和黄斑病变。
J Clin Invest. 2020 Jan 2;130(1):143-156. doi: 10.1172/JCI128513.
5
Mitochondrial single-stranded DNA binding protein novel de novo SSBP1 mutation in a child with single large-scale mtDNA deletion (SLSMD) clinically manifesting as Pearson, Kearns-Sayre, and Leigh syndromes.线粒体单链 DNA 结合蛋白新的从头 SSBP1 突变导致的单一大片段线粒体 DNA 缺失(SLSMD)患儿,临床表现为 Pearson、Kearns-Sayre 和 Leigh 综合征。
PLoS One. 2019 Sep 3;14(9):e0221829. doi: 10.1371/journal.pone.0221829. eCollection 2019.
6
SSBP1 mutations in dominant optic atrophy with variable retinal degeneration.SSBP1 突变导致的显性视神经萎缩伴视网膜变性的可变表现型。
Ann Neurol. 2019 Sep;86(3):368-383. doi: 10.1002/ana.25550. Epub 2019 Jul 31.
7
Mitochondrial fusion is required for regulation of mitochondrial DNA replication.线粒体融合对于调控线粒体 DNA 复制是必需的。
PLoS Genet. 2019 Jun 6;15(6):e1008085. doi: 10.1371/journal.pgen.1008085. eCollection 2019 Jun.
8
Deciphering OPA1 mutations pathogenicity by combined analysis of human, mouse and yeast cell models.通过对人、鼠和酵母细胞模型的综合分析来破译 OPA1 突变的致病性。
Biochim Biophys Acta Mol Basis Dis. 2018 Oct;1864(10):3496-3514. doi: 10.1016/j.bbadis.2018.08.004. Epub 2018 Aug 4.
9
Meta-analysis of genotype-phenotype analysis of OPA1 mutations in autosomal dominant optic atrophy.常染色体显性视神经萎缩 OPA1 突变的基因型-表型分析的荟萃分析。
Mitochondrion. 2019 May;46:262-269. doi: 10.1016/j.mito.2018.07.006. Epub 2018 Aug 27.
10
Heterozygous SSBP1 start loss mutation co-segregates with hearing loss and the m.1555A>G mtDNA variant in a large multigenerational family.杂合性 SSBP1 起始缺失突变与听力损失和 m.1555A>G 线粒体 DNA 变异在一个大型多代家族中共同遗传。
Brain. 2018 Jan 1;141(1):55-62. doi: 10.1093/brain/awx295.