Evidence map›Paper›PMID 26035391›Full record

ArticleDisease models & mechanisms2015

A mitochondrial therapeutic reverses visual decline in mouse models of diabetes.

Nazia M Alam, William C Mills, Aimee A Wong, Robert M Douglas, Hazel H Szeto, Glen T Prusky

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Disease models & mechanisms, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.7field-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

40 citing papers in PubMed, 55 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

6 authors at 3 institutions in 2 countries.

Nazia M AlamDepartment of Physiology and Biophysics, Weill Cornell Medical College, New York, NY, USA Burke Medical Research Institute, White Plains, NY, USA nma2006@med.cornell.edu.
William C MillsResearch Program in Mitochondrial Therapeutics, Department of Pharmacology, Weill Cornell Medical College, New York, NY, USA.
Aimee A WongBurke Medical Research Institute, White Plains, NY, USA.
Robert M DouglasDepartment of Ophthalmology and Visual Sciences, University of British Columbia, Vancouver, British Columbia, Canada.
Hazel H SzetoResearch Program in Mitochondrial Therapeutics, Department of Pharmacology, Weill Cornell Medical College, New York, NY, USA.
Glen T PruskyDepartment of Physiology and Biophysics, Weill Cornell Medical College, New York, NY, USA Burke Medical Research Institute, White Plains, NY, USA.
Cornell University · USBurke Medical Research Institute · USUniversity of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic retinopathy is characterized by progressive vision loss and the advancement of retinal micoraneurysms, edema and angiogenesis. Unfortunately, managing glycemia or targeting vascular complications with anti-vascular endothelial growth factor agents has shown only limited efficacy in treating the deterioration of vision in diabetic retinopathy. In light of growing evidence that mitochondrial dysfunction is an independent pathophysiology of diabetes and diabetic retinopathy, we investigated whether selectively targeting and improving mitochondrial dysfunction is a viable treatment for visual decline in diabetes. Measures of spatial visual behavior, blood glucose, bodyweight and optical clarity were made in mouse models of diabetes. Treatment groups were administered MTP-131, a water-soluble tetrapeptide that selectively targets mitochondrial cardiolipin and promotes efficient electron transfer, either systemically or in eye drops. Progressive visual decline emerged in untreated animals before the overt symptoms of metabolic and ophthalmic abnormalities were manifest, but with time, visual dysfunction was accompanied by compromised glucose clearance, and elevated blood glucose and bodyweight. MTP-131 treatment reversed the visual decline without improving glycemic control or reducing bodyweight. These data provide evidence that visuomotor decline is an early complication of diabetes. They also indicate that selectively treating mitochondrial dysfunction with MTP-131 has the potential to remediate the visual dysfunction and to complement existing treatments for diabetic retinopathy.

Indexed as

AnimalsBlood GlucoseDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Diabetic RetinopathyDisease Models, AnimalMaleMiceMice, Inbred C57BLMitochondriaMitochondrial DiseasesOligopeptidesOphthalmic SolutionsSensory ThresholdsVision, OcularVisual Perceptionarginyl-2,'6'-dimethyltyrosyl-lysyl-phenylalaninamideBlood GlucoseOligopeptidesOphthalmic SolutionsBendaviaCardiolipinDiabetic retinopathyHyperglycemiaInsulin resistanceMouseMTP-131OKTOptomotorRPESpatial visionSS-31

Identifiers

PMID26035391
PMCPMC4486862
OpenAlexW2239594936

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Registered trials

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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.