Evidence map›Paper›PMID 21978133›Full record

ReviewCurrent eye research2011

Mitochondrial dysfunction in retinal diseases.

Megha Barot, Mitan R Gokulgandhi, Ashim K Mitra

Open access · greenAbstract readReview
In one paragraph

Review in Current eye research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers.

0numbers the graph read from it
0cells of the map it votes in
120citing papers in PubMed
9.3field-weighted citation impact, top 2% 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

120 citing papers in PubMed, 181 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Mapping the Hypoxic Fitness Landscape of Retinal Pigment Epithelial Cells.International journal of molecular sciences · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. The Scavenging Activity of Coenzyme QInternational journal of molecular sciences · 2024
    Article
  18. Review
  19. Review
  20. Article

60 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Megha BarotSchool of Pharmacy, University of Missouri-Kansas City, Kansas City, MO 64108, USA.
Mitan R Gokulgandhi
Ashim K Mitra
University of Missouri–Kansas City · US

Funding

Ocular Disposition of Antimicrobial AgentsR01EY009171 · NEI · UNIVERSITY OF MISSOURI KANSAS CITY · PI MITRA, ASHIM K. · 1992 to 2010
$3.0M
Transscleral Transport & Polymeric Delivery of Antibody & Steroids for Macular EdR01EY010659 · NEI · UNIVERSITY OF MISSOURI KANSAS CITY · PI MITRA, ASHIM K. · 1996 to 2010
$2.5M
NEI NIH HHS R01 EY009171NEI NIH HHS R01 EY010659NEI NIH HHS R01 EY 09171-16NEI NIH HHS R01 EY 10659-14
6 · The paper itself

Abstract

The mitochondrion is a vital intracellular organelle for retinal cell function and survival. There is growing confirmation to support an association between mitochondrial dysfunction and a number of retinal degenerations. Investigations have also unveiled mitochondrial genomic instability as one of the contributing factors for age-related retinal pathophysiology. This review highlights the role of mitochondrial dysfunction originating from oxidative stress in the etiology of retinal diseases including diabetic retinopathy, glaucoma and age-related macular degeneration (AMD). Moreover, mitochondrial DNA (mtDNA) damage associated with AMD due to susceptibility of mtDNA to oxidative damage and failure of mtDNA repair pathways is also highlighted in this review. The susceptibility of neural retina and retinal pigment epithelium (RPE) mitochondria to oxidative damage with ageing appears to be a major factor in retinal degeneration. It thus appears that the mitochondrion is a weak link in the antioxidant defenses of retinal cells. In addition, failure of mtDNA repair pathways can also specifically contribute towards pathogenesis of AMD. This review will further summarize the prospective role of mitochondria targeting therapeutic agents for the treatment of retinal disease. Mitochondria based drug targeting to diminish oxidative stress or promote repair of mtDNA damage may offer potential alternatives for the treatment of various retinal degenerative diseases.

Indexed as

Oxidative StressDNA, MitochondrialHumansMitochondriaMitochondrial DiseasesRetinal DiseasesDNA, Mitochondrial

Identifiers

PMID21978133
PMCPMC4516173
OpenAlexW2071466648

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.