This article is a correction to:
The use of progeroid DNA repair-deficient mice for assessing anti-aging compounds, illustrating the benefits of nicotinamide riboside
María B. Birkisdóttir1,2
Ivar van Galen1,2
Renata M. C. Brandt3Sander Barnhoorn3Nicole van Vliet3
Claire van Dijk3,4Bhawani Nagarajah5Sandra Imholz5Conny T. van Oostrom5Erwin Reiling5Ákos Gyenis6
Pier G. Mastroberardino3,7,8
Dick Jaarsma9Harry van Steeg5Jan H. J. Hoeijmakers1,2,3,6
Martijn E. T. Dollé5*
Wilbert P. Vermeij1,2*- 1Princess Máxima Center for Pediatric Oncology, Utrecht, Netherlands
- 2Oncode Institute, Utrecht, Netherlands
- 3Department of Molecular Genetics, Erasmus MC Cancer Institute, Erasmus University Medical Center, Rotterdam, Netherlands
- 4Department of Hematology, Erasmus University Medical Center, Rotterdam, Netherlands
- 5Centre for Health Protection, National Institute for Public Health and the Environment, (RIVM), Bilthoven, Netherlands
- 6Faculty of Medicine, CECAD, Institute for Genome Stability in Aging and Disease, University of Cologne, Cologne, Germany
- 7IFOM-The FIRC Institute of Molecular Oncology, Milan, Italy
- 8Department of Life, Health, and Environmental Sciences, University of L'Aquila, L'Aquila, Italy
- 9Department of Neuroscience, Erasmus University Medical Center, Rotterdam, Netherlands
A Corrigendum on
The use of progeroid DNA repair-deficient mice for assessing anti-aging compounds, illustrating the benefits of nicotinamide riboside
by Birkisdóttir MB, van Galen I, Brandt RMC, Barnhoorn S, van Vliet N, van Dijk C, Nagarajah B, Imholz S, van Oostrom CT, Reiling E, Gyenis Á, Mastroberardino PG, Jaarsma D, van Steeg H, Hoeijmakers JHJ, Dollé MET and Vermeij WP (2022). Front. Aging 3:1005322. doi: 10.3389/fragi.2022.1005322
In the published article, there was an error in Figures 2, 3 as published. The panels in Figure 2 are labelled A, B, C, D, E, E, and F and in Figure 3 A, B, C, D, D, E, and F, while both were initially intended as A, B, C, D, E, F, G.
FIGURE 2
FIGURE 2. The effect of mitochondrial modifiers and GlcNAc supplementation on the lifespan and onset of neurological phenotypes of Ercc1Δ/− mice. (A–D), Comparison between Ercc1Δ/− control mice and animals supplemented with sodium nitrite, DCA, or GlcNAc on water intake (A), food intake (B), bodyweight over time (C) and body weight as area under the curve (AUC) of measurements between 6–16 weeks (D). (E–G), Onset of neurological abnormalities; tremors (E) and imbalance (F), and survival (G) of the same animals. Indicated values are Mean (±SD). Significant p values of the Dunnet’s multiple comparison test (A,E,F) are indicated.
FIGURE 3
FIGURE 3. The effect of nicotinamide ribosome supplementation on the lifespan and onset of neurological phenotypes of Ercc1Δ/− mice. (A–C), Values of water intake (A), food intake (B) body weight changes over time (C) and body weight as area under the curve (AUC) (D) in control animals and animals receiving supplementation of two NAD+ precursors; NA and NR. (E–F), Onset of neurological abnormalities; tremors (E) and imbalance (F) with age of Ercc1Δ/− control mice and mice receiving NR or NA. (G). Survival curve showing lifespan of the three groups. Indicated values are Mean (±SD). Significant p values of the Dunnet’s multiple comparison test (A) and log-rank survival test (F,G) are indicated.
The corrected Figures 2, 3 appear below.
The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.
Publisher’s note
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Keywords: aging, DNA damage repair, anti-aging interventions, pharmacological screening, dietary restriction mimetics, NAD, progeria
Citation: Birkisdóttir MB, van Galen I, Brandt RMC, Barnhoorn S, van Vliet N, van Dijk C, Nagarajah B, Imholz S, van Oostrom CT, Reiling E, Gyenis Á, Mastroberardino PG, Jaarsma D, van Steeg H, Hoeijmakers JHJ, Dollé MET and Vermeij WP (2022) Corrigendum: The use of progeroid DNA repair-deficient mice for assessing anti-aging compounds, illustrating the benefits of nicotinamide riboside. Front. Aging 3:1086552. doi: 10.3389/fragi.2022.1086552
Received: 01 November 2022; Accepted: 03 November 2022;
Published: 23 November 2022.
Approved by:
Frontiers Editorial Office, Frontiers Media SA, SwitzerlandCopyright © 2022 Birkisdóttir, van Galen, Brandt, Barnhoorn, van Vliet, van Dijk, Nagarajah, Imholz, van Oostrom, Reiling, Gyenis, Mastroberardino, Jaarsma, van Steeg, Hoeijmakers, Dollé and Vermeij. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Wilbert P. Vermeij, W.P.Vermeij@prinsesmaximacentrum.nl; Martijn E. T. Dollé, Martijn.Dolle@rivm.nl