Evidence map›Paper›PMID 34022179›Full record

ArticleThe American journal of pathology2021

Human RGR Gene and Associated Features of Age-Related Macular Degeneration in Models of Retina-Choriocapillaris Atrophy.

Xuan Bao, Zhaoxia Zhang, Yanjiang Guo, Christopher Buser, Harold Kochounian, Nancy Wu, Xiaohua Li, Shikun He, Bin Sun, Fred N Ross-Cisneros and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.9field-weighted citation impact, top 28% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Retinal G-protein-coupled receptor deletion exacerbates AMD-like changes via the PINK1-parkin pathway under oxidative stress.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  3. Article
  4. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 8 institutions in 2 countries.

Xuan BaoDepartment of Ophthalmology, Beijing Key Laboratory for the Diagnosis and Treatment of Retinal and Choroid Diseases, Peking University People's Hospital, Beijing, China; Department of Ophthalmology, Keck School of Medicine of USC, Los Angeles, California.
Zhaoxia ZhangDepartment of Ophthalmology, Keck School of Medicine of USC, Los Angeles, California; Shanxi Eye Hospital, Taiyuan, China.
Yanjiang GuoDepartment of Ophthalmology, Beijing Key Laboratory for the Diagnosis and Treatment of Retinal and Choroid Diseases, Peking University People's Hospital, Beijing, China.
Christopher BuserOak Crest Institute of Science, Monrovia, California.
Harold KochounianDoheny Eye Institute, Los Angeles, California.
Nancy WuNorris Cancer Center, Keck School of Medicine of University of Southern California, Los Angeles, California.
Xiaohua LiHenan Eye Institute, Henan Provincial People's Hospital, Henan, China.
Shikun HeDepartment of Pathology, Keck School of Medicine of USC, Los Angeles, California.
Bin SunShanxi Eye Hospital, Taiyuan, China.
Fred N Ross-CisnerosDoheny Eye Institute, Los Angeles, California.
Alfredo A SadunDoheny Eye Institute, Los Angeles, California; Department of Ophthalmology, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, California.
Lvzhen HuangDepartment of Ophthalmology, Beijing Key Laboratory for the Diagnosis and Treatment of Retinal and Choroid Diseases, Peking University People's Hospital, Beijing, China.
Mingwei ZhaoDepartment of Ophthalmology, Beijing Key Laboratory for the Diagnosis and Treatment of Retinal and Choroid Diseases, Peking University People's Hospital, Beijing, China. Electronic address: 0062011320@bjmu.edu.cn.
Henry K W FongDepartment of Ophthalmology, Keck School of Medicine of USC, Los Angeles, California; University of Southern California Roski Eye Institute, Los Angeles, California; Department of Molecular Microbiology and Immunology, University of Southern California, Los Angeles, California. Electronic address: hfong@usc.edu.
Peking University · CNDoheny Eye Institute · USKeck Hospital of USC · USUniversity of Southern California · USHenan Provincial People's Hospital · CNOak Crest Institute of Science · USShanxi Eye Hospital · CNUniversity of California, Los Angeles · US

Funding

Ophthalmic Therapeutics Engineering CoreP30EY029220 · NEI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI Mahnaz Shahidi · 2018 to 2026
$6.5M
OPSINS, G PROTEIN PATHWAYS AND REGULATION IN RPE CELLSR01EY008364 · NEI · DOHENY EYE INSTITUTE · PI FONG, HENRY K · 1990 to 2006
$2.5M
NEI NIH HHS P30 EY029220NEI NIH HHS R01 EY008364
6 · The paper itself

Abstract

Age-related macular degeneration (AMD) is a progressive eye disease and the most common cause of blindness among the elderly. AMD is characterized by early atrophy of the choriocapillaris and retinal pigment epithelium (RPE). Although AMD is a multifactorial disease with many environmental and genetic risk factors, a hallmark of the disease is the origination of extracellular deposits, or drusen, between the RPE and Bruch membrane. Human retinal G-protein-coupled receptor (RGR) gene generates an exon-skipping splice variant of RGR-opsin (RGR-d; NP_001012740) that is a persistent component of small and large drusen. Herein, the findings show that abnormal RGR proteins, including RGR-d, are pathogenic in an animal retina with degeneration of the choriocapillaris, RPE, and photoreceptors. A frameshift truncating mutation resulted in severe retinal degeneration with a continuous band of basal deposits along the Bruch membrane. RGR-d produced less severe disease with choriocapillaris and RPE atrophy, including focal accumulation of abnormal RGR-d protein at the basal boundary of the RPE. Degeneration of the choriocapillaris was marked by a decrease in endothelial CD31 protein and choriocapillaris breakdown at the ultrastructural level. Fundus lesions with patchy depigmentation were characteristic of old RGR-d mice. RGR-d was mislocalized in cultured cells and caused a strong cell growth defect. These results uphold the notion of a potential hidden link between AMD and a high-frequency RGR allele.

Indexed as

Disease Models, AnimalAnimalsAtrophyChoroidEye ProteinsHumansMacular DegenerationMiceReceptors, G-Protein-CoupledRetinaEye ProteinsG protein-coupled receptor RGRReceptors, G-Protein-Coupled

Identifiers

PMID34022179
PMCPMC8351129
OpenAlexW3160060986

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.