Evidence map›Paper›PMID 33246292›Full record

ReviewRedox biology2021

Targeting Nrf2 for the treatment of Duchenne Muscular Dystrophy.

Stephanie Kourakis, Cara A Timpani, Judy B de Haan, Nuri Gueven, Dirk Fischer, Emma Rybalka

Open access · goldAbstract readReview
In one paragraph

Review in Redox biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 48 citations in OpenAlex.

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  13. Adenylosuccinic Acid: An Orphan Drug with Untapped Potential.Pharmaceuticals (Basel, Switzerland) · 2023
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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 5 institutions in 2 countries.

Stephanie KourakisCollege of Health and Biomedicine, Victoria University, Melbourne, Victoria, Australia. Electronic address: stephanie.kourakis@live.vu.edu.au.
Cara A TimpaniInstitute for Health and Sport, Victoria University, Melbourne, Victoria, Australia; Australian Institute for Musculoskeletal Science, Victoria University, St Albans, Victoria, Australia. Electronic address: cara.timpani@vu.edu.au.
Judy B de HaanOxidative Stress Laboratory, Basic Science Domain, Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia; Department of Physiology, Anatomy and Microbiology, La Trobe University, Melbourne, Australia. Electronic address: judy.dehaan@baker.edu.au.
Nuri GuevenSchool of Pharmacy and Pharmacology, University of Tasmania, Hobart, Tasmania, Australia. Electronic address: nuri.guven@utas.edu.au.
Dirk FischerDivision of Developmental- and Neuropediatrics, University Children's Hospital Basel (UKBB), University of Basel, Basel, Switzerland. Electronic address: dirk.fischer@ukbb.ch.
Emma RybalkaCollege of Health and Biomedicine, Victoria University, Melbourne, Victoria, Australia; Institute for Health and Sport, Victoria University, Melbourne, Victoria, Australia; Australian Institute for Musculoskeletal Science, Victoria University, St Albans, Victoria, Australia. Electronic address: emma.rybalka@vu.edu.au.
Australian Institute for Musculoskeletal Science · AUBaker Heart and Diabetes Institute · AUUniversity of Basel · CHUniversity of Tasmania · AUVictoria University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Imbalances in redox homeostasis can result in oxidative stress, which is implicated in various pathological conditions including the fatal neuromuscular disease Duchenne Muscular Dystrophy (DMD). DMD is a complicated disease, with many druggable targets at the cellular and molecular level including calcium-mediated muscle degeneration; mitochondrial dysfunction; oxidative stress; inflammation; insufficient muscle regeneration and dysregulated protein and organelle maintenance. Previous investigative therapeutics tended to isolate and focus on just one of these targets and, consequently, therapeutic activity has been limited. Nuclear erythroid 2-related factor 2 (Nrf2) is a transcription factor that upregulates many cytoprotective gene products in response to oxidants and other toxic stressors. Unlike other strategies, targeted Nrf2 activation has the potential to simultaneously modulate separate pathological features of DMD to amplify therapeutic benefits. Here, we review the literature providing theoretical context for targeting Nrf2 as a disease modifying treatment against DMD.

Indexed as

Muscular Dystrophy, DuchenneAnimalsDisease Models, AnimalMiceMice, Inbred mdxMuscle, SkeletalNF-E2-Related Factor 2NF-E2-Related Factor 2Duchenne muscular dystrophyHormesisNrf2Oxidative stressReactive oxygen speciesSkeletal muscle

Identifiers

PMID33246292
PMCPMC7695875
OpenAlexW3109592327

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.