Evidence map›Paper›PMID 36521306›Full record

ArticleRedox biology2023

Decreased methylglyoxal-mediated protein glycation in the healthy aging mouse model of ectopic expression of UCP1 in skeletal muscle.

Jinit Masania, Patrick Wijten, Susanne Keipert, Mario Ost, Susanne Klaus, Naila Rabbani, Paul J Thornalley

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

Article in Redox biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Deciphering Uncoupling Proteins in Cellular Homeostasis and Metabolic Health.International journal of biological sciences · 2026
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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

7 authors at 5 institutions in 3 countries.

Jinit MasaniaClinical Sciences Research Laboratories, Warwick Medical School, University of Warwick, University Hospital, Coventry, CV2 2DX, UK.
Patrick WijtenDiabetes Research Center, Qatar Biomedical Research Institute, Hamad Bin Khalifa University, Qatar Foundation, P.O. Box 34110, Doha, Qatar.
Susanne KeipertDepartment of Physiology of Energy Metabolism, German Institute of Human Nutrition, Potsdam-Rehbruecke, 14558, Nuthetal, Germany.
Mario OstDepartment of Physiology of Energy Metabolism, German Institute of Human Nutrition, Potsdam-Rehbruecke, 14558, Nuthetal, Germany.
Susanne KlausDepartment of Physiology of Energy Metabolism, German Institute of Human Nutrition, Potsdam-Rehbruecke, 14558, Nuthetal, Germany; University of Potsdam, Institute of Nutrition Science, Potsdam-Rehbruecke, 14558, Nuthetal, Germany.
Naila RabbaniDepartment of Basic Medical Science, College of Medicine, QU Health, Qatar University, P.O. Box 2713, Doha, Qatar.
Paul J ThornalleyClinical Sciences Research Laboratories, Warwick Medical School, University of Warwick, University Hospital, Coventry, CV2 2DX, UK; Diabetes Research Center, Qatar Biomedical Research Institute, Hamad Bin Khalifa University, Qatar Foundation, P.O. Box 34110, Doha, Qatar. Electronic address: pthornalley@hbku.edu.qa.
German Institute of Human Nutrition · DEUniversity Hospital Coventry · GBHamad bin Khalifa University · QAQatar University · QAUniversity of Potsdam · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mice with ectopic expression of uncoupling protein-1 (UCP1) in skeletal muscle exhibit a healthy aging phenotype with increased longevity and resistance to impaired metabolic health. This may be achieved by decreasing protein glycation by the reactive metabolite, methylglyoxal (MG). We investigated protein glycation and oxidative damage in skeletal muscle of mice with UCP1 expression under control of the human skeletal actin promoter (HSA-mUCP1) at age 12 weeks (young) and 70 weeks (aged). We found both young and aged HSA-mUCP1 mice had decreased advanced glycation endproducts (AGEs) formed from MG, lysine-derived N

Indexed as

Glycation End Products, AdvancedHealthy AgingAgedAnimalsEctopic Gene ExpressionHumansInfantLysineMaillard ReactionMiceMuscle, SkeletalProteinsPyruvaldehydeTumor Suppressor ProteinsUbiquitin-Protein LigasesUncoupling Protein 1Glycation End Products, AdvancedHUWE1 protein, humanLysineProteinsPyruvaldehydeTumor Suppressor ProteinsUbiquitin-Protein LigasesUCP1 protein, humanUcp1 protein, mouseUncoupling Protein 1AgingMethylglyoxalProtein glycationProteomicsSkeletal muscleUncoupling protein 1

Identifiers

PMID36521306
PMCPMC9772855
OpenAlexW4310758480

What OpenQuestion holds

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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.