Evidence map›Paper›PMID 29436254›Full record

ReviewExpert opinion on therapeutic targets2018

Therapeutic targets for altering mitochondrial dysfunction associated with diabetic retinopathy.

Renu A Kowluru, Manish Mishra

Open access · greenAbstract readReview
In one paragraph

Review in Expert opinion on therapeutic targets, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.6field-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

31 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. New perspectives on DNA methylation modifications in ocular diseases.International journal of ophthalmology · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Epigenetic modifications in diabetes.Metabolism: clinical and experimental · 2022
    Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Mitophagy in Human Diseases.International journal of molecular sciences · 2021
    Review
  18. Review
  19. Review
  20. 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

2 authors at 2 institutions in 1 country.

Renu A Kowlurua Department of Ophthalmology, Kresge Eye Institute , Wayne State University , Detroit , MI , USA.
Manish Mishraa Department of Ophthalmology, Kresge Eye Institute , Wayne State University , Detroit , MI , USA.
Kresge Eye Institute · USWayne State University · US

Funding

Role of Ras in Retinal Cell Death in DiabetesR01EY014370 · NEI · WAYNE STATE UNIVERSITY · PI KOWLURU, RENU A. · 2004 to 2023
$4.8M
Glycemic Control and Progression of Diabetic RetinopathyR01EY017313 · NEI · WAYNE STATE UNIVERSITY · PI KOWLURU, RENU A. · 2007 to 2022
$4.2M
NADPH Oxidase, Mitochondrial Dysfunction and Diabetic RetinopathyR01EY022230 · NEI · WAYNE STATE UNIVERSITY · PI KOWLURU, ANJANEYULU, KOWLURU, RENU A. · 2012 to 2022
$3.4M
NEI NIH HHS R01 EY014370NEI NIH HHS R01 EY017313NEI NIH HHS R01 EY022230
6 · The paper itself

Abstract

introductionRetinopathy remains as one of the most feared blinding complications of diabetes, and with the prevalence of this life-long disease escalating at an alarming rate, the incidence of retinopathy is also climbing. Although the cutting edge research has identified many molecular mechanisms associated with its development, the exact mechanism how diabetes damages the retina remains obscure, limiting therapeutic options for this devastating disease. Areas covered: This review focuses on the central role of mitochondrial dysfunction/damage in the pathogenesis of diabetic retinopathy, and how damaged mitochondria initiates a self-perpetuating vicious cycles of free radicals. We have also reviewed how mitochondria could serve as a therapeutic target, and the challenges associated with the complex double mitochondrial membranes and a well-defined blood-retinal barrier for optimal pharmacologic/molecular approach to improve mitochondrial function. Expert opinion: Mitochondrial dysfunction provides many therapeutic targets for ameliorating the development of diabetic retinopathy including their biogenesis, DNA damage and epigenetic modifications. New technology to enhance pharmaceuticals uptake inside the mitochondria, nanotechnology to deliver drugs to the retina, and maintenance of mitochondrial homeostasis via lifestyle changes and novel therapeutics to prevent epigenetic modifications, could serve as some of the welcoming avenues for a diabetic patient to target this sight-threatening disease.

Indexed as

Molecular Targeted TherapyAnimalsDiabetic RetinopathyDNA DamageDrug Delivery SystemsDrug DesignEpigenesis, GeneticFree RadicalsHumansLife StyleMitochondriaNanotechnologyFree RadicalsDiabetesdiabetic retinopathyepigeneticsmitochondriamitochondrial DNAreactive oxygen speciesretina

Identifiers

PMID29436254
PMCPMC6088375
OpenAlexW2793196984

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.