Evidence map›Paper›PMID 26756334›Full record

ArticlePloS one2016

Nmnat3 Is Dispensable in Mitochondrial NAD Level Maintenance In Vivo.

Masashi Yamamoto, Keisuke Hikosaka, Arshad Mahmood, Kazuyuki Tobe, Hideo Shojaku, Hidenori Inohara, Takashi Nakagawa

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
5.3field-weighted citation impact, top 5% 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

45 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Article
  3. Mitochondrial NMNAT3 reduces amyloid aggregates inMitochondrial communications · 2026
    Article
  4. Review
  5. Review
  6. Article
  7. The role of NADnpj metabolic health and disease · 2025
    Review
  8. Article
  9. Emerging interactions between mitochondria and NADTrends in endocrinology and metabolism: TEM · 2025
    Review
  10. Subcellular NADNature metabolism · 2024
    Article
  11. Article
  12. Regulation of and challenges in targeting NADNature reviews. Molecular cell biology · 2024
    Review
  13. Inhibitors of NADInternational journal of molecular sciences · 2024
    Review
  14. Roles of NADCold Spring Harbor perspectives in medicine · 2024
    Review
  15. Review
  16. Harnessing NADCurrent heart failure reports · 2022
    Review
  17. Review
  18. Fueling genome maintenance: On the versatile roles of NADThe Journal of biological chemistry · 2022
    Review
  19. Article
  20. Nuclear NADScience advances · 2021
    Article
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 2 institutions in 1 country.

Masashi YamamotoFrontier Research Core for Life Sciences, University of Toyama, Toyama 930-0194, Japan.
Keisuke HikosakaFrontier Research Core for Life Sciences, University of Toyama, Toyama 930-0194, Japan.
Arshad MahmoodFrontier Research Core for Life Sciences, University of Toyama, Toyama 930-0194, Japan.
Kazuyuki TobeFirst Department of Internal Medicine, Graduate School of Medicine and Pharmaceutical Science for Research, University of Toyama, Toyama 930-0194, Japan.
Hideo ShojakuDepartment of Otorhinolaryngology, Head and Neck Surgery, Graduate School of Medicine and Pharmaceutical Science for Research, University of Toyama, Toyama 930-0194, Japan.
Hidenori InoharaDepartment of Otorhinolaryngology-Head and Neck Surgery, Osaka University Graduate School of Medicine, Osaka 565-0871, Japan.
Takashi NakagawaFrontier Research Core for Life Sciences, University of Toyama, Toyama 930-0194, Japan.
University of Toyama · JPOsaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nicotinamide adenine dinucleotide (NAD) is an essential co-enzyme mediating various enzymatic reactions. Mitochondrial NAD particularly occupies a considerable amount of total NAD in cells, and serves as a co-enzyme in tricarboxylic acid cycle (TCA cycle), β-oxidation, and oxidative phosphorylation. Despite the importance of mitochondrial NAD, its synthesis pathway remains unknown. It has been proposed that NAD synthesis enzyme, Nmnat3, was localized in mitochondria, but its physiological relevance to the metabolism in mitochondria was not fully elucidated. Previously, we have reported that murine Nmnat3 protein was strongly expressed in the cytoplasm of mature erythrocytes, in which mitochondria were absent, and Nmnat3-deficient mice (Nmnat3-KO mice) exhibited splenomegaly and hemolytic anemia due to reduced NAD levels in mature erythrocytes. These results challenged the role of Nmnat3 in mitochondrial NAD synthesis. In this study, we demonstrated that mitochondrial NAD levels in various tissues, except for red blood cells, were unchanged in Nmnat3-KO mice. We also analyzed the metabolites in glycolysis and TCA cycle and found that there were no differences between Nmnat3-KO and WT mice. In addition, the aged Nmnat3-KO mice had comparable NAD levels to that observed in WT mice. Our results indicated that Nmnat3 is dispensable in the maintenance of mitochondrial NAD levels, and that other NAD regulatory pathways may exist in mitochondria.

Indexed as

AnimalsMiceMice, KnockoutMitochondriaNADNicotinamide-Nucleotide AdenylyltransferaseNADnicotinamide mononucleotide adenylyltransferase 3, mouseNicotinamide-Nucleotide Adenylyltransferase

Identifiers

PMID26756334
PMCPMC4710499
OpenAlexW2236926495

What OpenQuestion holds

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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.