Evidence map›Paper›PMID 37485393›Full record

ArticleFrontiers in nutrition2023

Maternal protein deficiency alters primary cilia length in renal tubular and impairs kidney development in fetal rat.

Jun Wang, Pei Zhou, Liangliang Zhu, Hongbo Guan, Jian Gou, Xiaomei Liu

Abstract read
In one paragraph

Article in Frontiers in nutrition, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Ciliary and Non-Ciliary Roles of IFT88 in Development and Diseases.International journal of molecular sciences · 2025
    Review
  7. Review
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

6 authors.

Jun WangDepartment of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang, China.
Pei ZhouDepartment of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang, China.
Liangliang ZhuDepartment of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang, China.
Hongbo GuanDepartment of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang, China.
Jian GouDepartment of Nutrition, Shengjing Hospital of China Medical University, Shenyang, China.
Xiaomei LiuDepartment of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Intrauterine malnutrition impairs embryo kidney development and leads to kidney disease and hypertension in adulthood, yet the underlying mechanism remains unclear. Methods: With a maternal protein restriction (MPR) rat model, we investigated the critical ciliogenesis factors and β-catenin pathway in FGR fetal kidneys and analyzed the impact of aberrant primary cilia on renal tubular epithelium. Results: The data showed decreased nephron number and renal tubular dysgenesis in FGR fetus. FGR fetus showed deregulated expression of ciliogenesis factors including upregulation of IFT88 and downregulation of DYNLT1, accompanied with cilia elongation in renal tubular epithelial cells. Wnt7b, the key ligand for Wnt/β-catenin signaling, was downregulated and nuclear translocation of β-catenin was decreased. The proapoptotic protein was upregulated. Discussion: We elucidated that intrauterine protein malnutrition led to deregulation of ciliogenesis factors and cilia elongation in renal tubular epithelial, inhibited β-catenin signaling, and induced cell apoptosis and ultimately, compromised kidney development.

Indexed as

DYNLT1FGRIFT88kidneyprimary ciliaβ-catenin pathway

Identifiers

PMID37485393
PMCPMC10358357

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