Evidence map›Paper›PMID 28060768›Full record

ArticleOncotarget2017

A novel osteoporosis model with ascorbic acid deficiency in Akr1A1 gene knockout mice.

Cheng-Wei Lai, Hsiao-Ling Chen, Min-Yu Tu, Wei-Yu Lin, Theresa Röhrig, Shang-Hsun Yang, Ying-Wei Lan, Kowit-Yu Chong, Chuan-Mu Chen

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

14 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  5. Commentary: Lactylation-related geneFrontiers in immunology · 2025
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  7. Vitamin C Deficiency Deteriorates Bone Microarchitecture and Mineralization in a Sex-Specific Manner in Adult Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023
    Article
  8. Article
  9. Review
  10. Ascorbate Is a Primary Antioxidant in Mammals.Molecules (Basel, Switzerland) · 2022
    Review
  11. Article
  12. Review
  13. Article
  14. Oral immunotherapy with the ingestion of house dust mite extract in a murine model of allergic asthma.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2018
    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

9 authors at 5 institutions in 1 country.

Cheng-Wei LaiDepartment of Life Sciences, National Chung Hsing University, Taichung, Taiwan.
Hsiao-Ling ChenDepartment of Bioresources, Da-Yeh University, Changhua, Taiwan.
Min-Yu TuDepartment of Life Sciences, National Chung Hsing University, Taichung, Taiwan.
Wei-Yu LinDepartment of Life Sciences, National Chung Hsing University, Taichung, Taiwan.
Theresa RöhrigDepartment of Life Sciences, National Chung Hsing University, Taichung, Taiwan.
Shang-Hsun YangDepartment of Physiology and Institute of Basic Medical Sciences, National Cheng Kung University, Tainan, Taiwan.
Ying-Wei LanDepartment of Life Sciences, National Chung Hsing University, Taichung, Taiwan.
Kowit-Yu ChongDepartment of Medical Biotechnology and Laboratory Science, College of Medicine, Chang Gung University, Tao-Yuan, Taiwan.
Chuan-Mu ChenDepartment of Life Sciences, National Chung Hsing University, Taichung, Taiwan.
National Chung Hsing University · TWChang Gung University · TWDayeh University · TWNational Cheng Kung University · TWNational Defense Medical Center · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The AKR1A1 protein is a member of the aldo-keto reductase superfamily that is responsible for the conversion of D-glucuronate to L-gulonate in the ascorbic acid (vitamin C) synthesis pathway. In a pCAG-eGFP transgenic mouse line that was produced by pronuclear microinjection, the integration of the transgene resulted in a 30-kb genomic DNA deletion, including the Akr1A1 gene, and thus caused the knockout (KO) of the Akr1A1 gene and targeting of the eGFP gene. The Akr1A1 KO mice (Akr1A1eGFP/eGFP) exhibited insufficient serum ascorbic acid levels, abnormal bone development and osteoporosis. Using micro-CT analysis, the results showed that the microarchitecture of the 12-week-old Akr1A1eGFP/eGFP mouse femur was shorter in length and exhibited less cortical bone thickness, enlargement of the bone marrow cavity and a complete loss of the trabecular bone in the distal femur. The femoral head and neck of the proximal femur also showed a severe loss of bone mass. Based on the decreased levels of serum osteocalcin and osteoblast activity in the Akr1A1eGFP/eGFP mice, the osteoporosis might be caused by impaired bone formation. In addition, administration of ascorbic acid to the Akr1A1eGFP/eGFP mice significantly prevented the condition of osteoporotic femurs and increased bone formation. Therefore, through ascorbic acid administration, the Akr1A1 KO mice exhibited controllable osteoporosis and may serve as a novel model for osteoporotic research.

Indexed as

Gene Knockout TechniquesOsteogenesisAldehyde ReductaseAnimalsAscorbic AcidAscorbic Acid DeficiencyDisease Models, AnimalFemaleFemurGenetic Predisposition to DiseaseMice, KnockoutOsteoblastsOsteocalcinOsteoporosisPhenotypeTime FactorsAldehyde ReductaseAscorbic AcidOsteocalcinAkr1A1 geneascorbic acidcortical boneknockout micemicro-CT imagingosteoporosisPathology Sectiontrabecular bone

Identifiers

PMID28060768
PMCPMC5352327
OpenAlexW2565847609

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.