Evidence map›Paper›PMID 33930395›Full record

ReviewExperimental eye research2021

Ongoing controversies and recent insights of the ARMS2-HTRA1 locus in age-related macular degeneration.

Adam May, Fei Su, Brian Dinh, Rachael Ehlen, Christina Tran, Harini Adivikolanu, Peter X Shaw

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Experimental eye research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  12. The interactions betweenMolecular vision · 2024
    Article
  13. CRISPR editing demonstrates rs10490924 raised oxidative stress in iPSC-derived retinal cells from patients withProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  14. Review
  15. Article
  16. Article
  17. Role ofTaiwan journal of ophthalmology
    Review
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

7 authors at 1 institution in 1 country.

Adam MayViterbi Family Department of Ophthalmology and Shiley Eye Institute, University of California, San Diego, 9415 Campus Point Drive, La Jolla, CA 92093-0946, USA; Altman Clinical and Translational Research Institute, University of California, San Diego, 9452 Medical Center Drive, La Jolla, CA 92093-0990, USA. Electronic address: a5may@ucsd.edu.
Fei SuViterbi Family Department of Ophthalmology and Shiley Eye Institute, University of California, San Diego, 9415 Campus Point Drive, La Jolla, CA 92093-0946, USA; Altman Clinical and Translational Research Institute, University of California, San Diego, 9452 Medical Center Drive, La Jolla, CA 92093-0990, USA. Electronic address: sophiasucn@gmail.com.
Brian DinhViterbi Family Department of Ophthalmology and Shiley Eye Institute, University of California, San Diego, 9415 Campus Point Drive, La Jolla, CA 92093-0946, USA; Altman Clinical and Translational Research Institute, University of California, San Diego, 9452 Medical Center Drive, La Jolla, CA 92093-0990, USA. Electronic address: btdinh@ucsd.edu.
Rachael EhlenViterbi Family Department of Ophthalmology and Shiley Eye Institute, University of California, San Diego, 9415 Campus Point Drive, La Jolla, CA 92093-0946, USA; Altman Clinical and Translational Research Institute, University of California, San Diego, 9452 Medical Center Drive, La Jolla, CA 92093-0990, USA. Electronic address: rachael.ehlen@gmail.com.
Christina TranViterbi Family Department of Ophthalmology and Shiley Eye Institute, University of California, San Diego, 9415 Campus Point Drive, La Jolla, CA 92093-0946, USA; Altman Clinical and Translational Research Institute, University of California, San Diego, 9452 Medical Center Drive, La Jolla, CA 92093-0990, USA. Electronic address: cdtran@ucsd.edu.
Harini AdivikolanuViterbi Family Department of Ophthalmology and Shiley Eye Institute, University of California, San Diego, 9415 Campus Point Drive, La Jolla, CA 92093-0946, USA; Altman Clinical and Translational Research Institute, University of California, San Diego, 9452 Medical Center Drive, La Jolla, CA 92093-0990, USA. Electronic address: hadiviko@ucsd.edu.
Peter X ShawViterbi Family Department of Ophthalmology and Shiley Eye Institute, University of California, San Diego, 9415 Campus Point Drive, La Jolla, CA 92093-0946, USA; Altman Clinical and Translational Research Institute, University of California, San Diego, 9452 Medical Center Drive, La Jolla, CA 92093-0990, USA. Electronic address: pshaw@ucsd.edu.
University of California San Diego · US

Funding

Vision BiostatisticsP30EY022589 · NEI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Radha Ayyagari · 2012 to 2026
$10.3M
HTRA1 as a Therapeutic Target in the Treatment of Wet AMDR01EY025693 · NEI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SHAW, PETER X · 2015 to 2019
$1.8M
NEI NIH HHS P30 EY022589NEI NIH HHS R01 EY025693
6 · The paper itself

Abstract

Age-related macular degeneration (AMD) is the most common cause of central vision loss among elderly populations in industrialized countries. Genome-wide association studies have consistently associated two genomic loci with progression to late-stage AMD: the complement factor H (CFH) locus on chromosome 1q31 and the age-related maculopathy susceptibility 2-HtrA serine peptidase 1 (ARMS2-HTRA1) locus on chromosome 10q26. While the CFH risk variant has been shown to alter complement activity, the ARMS2-HTRA1 risk haplotype remains enigmatic due to high linkage disequilibrium and inconsistent functional findings spanning two genes that are plausibly causative for AMD risk. In this review, we detail the genetic and functional evidence used to support either ARMS2 or HTRA1 as the causal gene for AMD risk, emphasizing both the historical development and the current understanding of the ARMS2-HTRA1 locus in AMD pathogenesis. We conclude by summarizing the evidence in favor of HTRA1 and present our hypothesis whereby HTRA1-derived ECM fragments mediate AMD pathogenesis.

Indexed as

Chromosomes, Human, Pair 10Genetic LociGenome-Wide Association StudyHaplotypesHigh-Temperature Requirement A Serine Peptidase 1HumansLinkage DisequilibriumMacular DegenerationProteinsARMS2 protein, humanHigh-Temperature Requirement A Serine Peptidase 1HTRA1 protein, humanProteinsAge-related macular degenerationARMS2-HTRA1 gene locusComplement systemExtracellular matrixLinkage disequilibriumTGF-Beta signaling

Identifiers

PMID33930395
PMCPMC12053538
OpenAlexW3157313869

What OpenQuestion holds

Textmetadata
LicenceTDM
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.