Evidence map›Paper›PMID 33162377›Full record

ReviewRedox biology2020

Complement activation, lipid metabolism, and mitochondrial injury: Converging pathways in age-related macular degeneration.

Li Xuan Tan, Colin J Germer, Nilsa La Cunza, Aparna Lakkaraju

Open access · goldAbstract readReview
In one paragraph

Review in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Li Xuan TanDepartment of Ophthalmology, School of Medicine, University of California, San Francisco, CA, USA.
Colin J GermerDepartment of Ophthalmology, School of Medicine, University of California, San Francisco, CA, USA; Pharmaceutical Sciences and Pharmacogenomics Graduate Program, University of California, San Francisco, CA, USA.
Nilsa La CunzaDepartment of Ophthalmology, School of Medicine, University of California, San Francisco, CA, USA; Pharmaceutical Sciences and Pharmacogenomics Graduate Program, University of California, San Francisco, CA, USA.
Aparna LakkarajuDepartment of Ophthalmology, School of Medicine, University of California, San Francisco, CA, USA; Pharmaceutical Sciences and Pharmacogenomics Graduate Program, University of California, San Francisco, CA, USA; Department of Anatomy, School of Medicine, University of California, San Francisco, CA, USA. Electronic address: Aparna.Lakkaraju@ucsf.edu.
University of California, San Francisco · US

Funding

Rapid-Prototyping and Design CoreP30EY002162 · NEI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ULLIAN, ERIK M · 1985 to 2024
$16.8M
University of Michigan Postbaccalaureate Research Education Program (UM PREP)R25GM086262 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ALLEN, BENJAMIN · 2009 to 2024
$6.1M
Mechanisms of RPE dysfunction in macular degenerations: role of intracellular complement activationR01EY030668 · NEI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LAKKARAJU, APARNA · 2020 to 2024
$3.5M
Mechanisms of cellular clearance in the retinal pigment epitheliumR01EY023299 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI LAKKARAJU, APARNA · 2015 to 2019
$2.3M
NEI NIH HHS P30 EY002162NEI NIH HHS R01 EY023299NEI NIH HHS R01 EY030668NIGMS NIH HHS R25 GM086262
6 · The paper itself

Abstract

The retinal pigment epithelium (RPE) is the primary site of injury in non-neovascular age-related macular degeneration or dry AMD. Polymorphisms in genes that regulate complement activation and cholesterol metabolism are strongly associated with AMD, but the biology underlying disease-associated variants is not well understood. Here, we highlight recent studies that have used molecular, biochemical, and live-cell imaging methods to elucidate mechanisms by which aging-associated insults conspire with AMD genetic risk variants to tip the balance towards disease. We discuss how critical functions including lipid metabolism, autophagy, complement regulation, and mitochondrial dynamics are compromised in the RPE, and how a deeper understanding of these mechanisms has helped identify promising therapeutic targets to preserve RPE homeostasis in AMD.

Indexed as

Lipid MetabolismMacular DegenerationComplement ActivationHumansMitochondriaRetinal Pigment EpitheliumAutophagyCeramideCholesterolComplementMitochondriaRetinal pigment epithelium

Identifiers

PMID33162377
PMCPMC7767764
OpenAlexW3097189385

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.