Evidence map›Paper›PMID 29291141›Full record

ReviewBioResearch open access2017

Epigenetic Treatment of Neurodegenerative Ophthalmic Disorders: An Eye Toward the Future.

Walter H Moos, Douglas V Faller, Ioannis P Glavas, David N Harpp, Michael H Irwin, Iphigenia Kanara, Carl A Pinkert, Whitney R Powers, Kosta Steliou, Demetrios G Vavvas and 1 more

Open access · diamondAbstract readReview
In one paragraph

Review in BioResearch open access, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

5 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. 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

11 authors at 8 institutions in 2 countries.

Walter H MoosDepartment of Pharmaceutical Chemistry, School of Pharmacy, University of California San Francisco, San Francisco, California.
Douglas V FallerDepartment of Medicine, Boston University School of Medicine, Boston, Massachusetts.
Ioannis P GlavasDepartment of Ophthalmology, New York University School of Medicine, New York, New York.
David N HarppDepartment of Chemistry, McGill University, Montreal, QC, Canada.
Michael H IrwinDepartment of Pathobiology, College of Veterinary Medicine, Auburn University, Auburn, Alabama.
Iphigenia KanaraEmbassy of Greece in Moscow, Moscow, Russia.
Carl A PinkertDepartment of Biological Sciences, College of Arts and Sciences, The University of Alabama, Tuscaloosa, Alabama.
Whitney R PowersDepartment of Health Sciences, Boston University, Boston, Massachusetts.
Kosta SteliouCancer Research Center, Boston University School of Medicine, Boston, Massachusetts.
Demetrios G VavvasRetina Service, Angiogenesis Laboratory, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts.
Krishna KodukulaShangPharma Innovation, Inc., South San Francisco, California.
Boston University · USAuburn University · USBridgewater College · USMassachusetts Eye and Ear Infirmary · USMcGill University · CANew York University · USUniversity of Alabama · USUniversity of California, San Francisco · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Eye disease is one of the primary medical conditions that requires attention and therapeutic intervention in ageing populations worldwide. Further, the global burden of diabetes and obesity, along with heart disease, all lead to secondary manifestations of ophthalmic distress. Therefore, there is increased interest in developing innovative new approaches that target various mechanisms and sequelae driving conditions that result in adverse vision. The research challenge is even greater given that the terrain of eye diseases is difficult to landscape into a single therapeutic theme. This report addresses the burden of eye disease due to mitochondrial dysfunction, including antioxidant, autophagic, epigenetic, mitophagic, and other cellular processes that modulate the biomedical end result. In this light, we single out lipoic acid as a potent known natural activator of these pathways, along with alternative and potentially more effective conjugates, which together harness the necessary potency, specificity, and biodistribution parameters required for improved therapeutic outcomes.

Indexed as

antioxidantcarnitinelipoic acidmacular degenerationmitochondriaretina

Identifiers

PMID29291141
PMCPMC5747116
OpenAlexW2782451016

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.