ArticleFree radical biology & medicine2019
Loss of methionine sulfoxide reductases increases resistance to oxidative stress.
Article in Free radical biology & medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.
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.
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.
Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- Physical exercise as a precision strategy for targeted PINK1 recruitment- a mechanistic review.Frontiers in physiology · 2026Review
- Tissue-specific molecular regulation of aging mechanisms with methionine restriction in mice and the potential role of methionine sulfoxide reductase.The journals of gerontology. Series A, Biological sciences and medical sciences · 2025Article
- The Interplay between Endogenous and Foodborne Pro-Oxidants and Antioxidants in Shaping Redox Homeostasis.International journal of molecular sciences · 2024Review
- Response to oxidative stress of AML12 hepatocyte cells with knockout of methionine sulfoxide reductases.Free radical biology & medicine · 2023Article
- Biological and Catalytic Properties of Selenoproteins.International journal of molecular sciences · 2023Review
- Metamorphism in TDP-43 prion-like domain determines chaperone recognition.Nature communications · 2023Article
- Article
- Metabolic benefits of methionine restriction in adult mice do not require functional methionine sulfoxide reductase A (MsrA).Scientific reports · 2022Article
- Fluorescent probes for visualizing ROS-associated proteins in disease.Chemical science · 2021Review
- Mitochondrial Redox Signaling and Oxidative Stress in Kidney Diseases.Biomolecules · 2021Review
- Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Oxidation of methionine residues to methionine sulfoxide scavenges reactive species, thus protecting against oxidative stress. Reduction of the sulfoxide back to methionine by methionine sulfoxide reductases creates a cycle with catalytic efficiency. Protection by the methionine sulfoxide reductases is well documented in cultured cells, from microorganisms to mammals. However, knocking out one or two of the 4 mammalian reductases had little effect in mice that were not stressed. We hypothesized that the minimal effect is due to redundancy provided by the 4 reductases. We tested the hypothesis by creating a transgenic mouse line lacking all 4 reductases and predicted that this mouse would be exceptionally sensitive to oxidative stress. The mutant mice were phenotypically normal at birth, exhibited normal post-natal growth, and were fertile. Surprisingly, rather than being more sensitive to oxidative stress, they were more resistant to both cardiac ischemia-reperfusion injury and to parenteral paraquat, a redox-cycling agent. Resistance was not a result of hormetic induction of the antioxidant transcription factor Nrf2 nor activation of Akt. The mechanism of protection may be novel.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.