Evidence map›Paper›PMID 41977230›Full record

ArticleInternational journal of molecular sciences2026

Vitamin D Deficiency Activates Gdnf-Ret-pErk1/2 Signal and Induces Kidney Malformations in Mice.

Minghui Yu, Ningli Ye, Haixin Ju, Qianfan Miao, Chunyan Wang, Rufeng Dai, Jing Chen, Yihui Zhai, Lei Sun, Xiaohui Wu and 2 more

Abstract read
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In one paragraph

Article in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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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

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0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Minghui YuDepartment of Nephrology, Children's Hospital of Fudan University, Shanghai Kidney Development and Pediatric Kidney Disease Research Center, National Children's Medical Center, Shanghai 201102, China.
Ningli YeDepartment of Nephrology, Children's Hospital of Fudan University, Shanghai Kidney Development and Pediatric Kidney Disease Research Center, National Children's Medical Center, Shanghai 201102, China.
Haixin JuDepartment of Nephrology, Children's Hospital of Fudan University, Shanghai Kidney Development and Pediatric Kidney Disease Research Center, National Children's Medical Center, Shanghai 201102, China.
Qianfan MiaoDepartment of Nephrology, Children's Hospital of Fudan University, Shanghai Kidney Development and Pediatric Kidney Disease Research Center, National Children's Medical Center, Shanghai 201102, China.
Chunyan WangDepartment of Nephrology, Children's Hospital of Fudan University, Shanghai Kidney Development and Pediatric Kidney Disease Research Center, National Children's Medical Center, Shanghai 201102, China.
Rufeng DaiDepartment of Nephrology, Children's Hospital of Fudan University, Shanghai Kidney Development and Pediatric Kidney Disease Research Center, National Children's Medical Center, Shanghai 201102, China.
Jing ChenDepartment of Nephrology, Children's Hospital of Fudan University, Shanghai Kidney Development and Pediatric Kidney Disease Research Center, National Children's Medical Center, Shanghai 201102, China.
Yihui ZhaiDepartment of Nephrology, Children's Hospital of Fudan University, Shanghai Kidney Development and Pediatric Kidney Disease Research Center, National Children's Medical Center, Shanghai 201102, China.
Lei SunState Key Laboratory of Genetic Engineering and National Center for International Research of Development and Disease, Institute of Developmental Biology and Molecular Medicine, Collaborative Innovation Center of Genetics and Development, School of Life Sciences, Fudan University, Shanghai 200032, China.
Xiaohui WuSchool of Basic Medical Sciences, Shanghai University of Medicine and Health Sciences, Shanghai 201318, China.
Hong XuDepartment of Nephrology, Children's Hospital of Fudan University, Shanghai Kidney Development and Pediatric Kidney Disease Research Center, National Children's Medical Center, Shanghai 201102, China.
Qian ShenDepartment of Nephrology, Children's Hospital of Fudan University, Shanghai Kidney Development and Pediatric Kidney Disease Research Center, National Children's Medical Center, Shanghai 201102, China.ORCID 0000-0003-3056-6737

Funding

National Key Research and Development Program of China No.2022YFC2705100, 2022YFC2705105National Key Research and Development Program of China No.2024YFC3406700, 2024YFC3406705National Natural Science Foundation of China 82470707Shanghai "Science and Technology Innovation Action Plan" (Sailing Special Project) 22YF1403600
6 · The paper itself

Abstract

Congenital anomalies of the kidney and urinary tract (CAKUT) constitute the most common underlying cause of chronic kidney disease in pediatric populations. Maternal hypovitaminosis D links to mesoderm-related birth defects, leading to our hypothesis that maternal vitamin D deficiency (VDD) impairs renal development (a mesoderm-derived process) and induces offspring CAKUT. To investigate whether a low-vitamin D level can cause CAKUT, we used vitamin D-free diets to induce a maternal vitamin D deficiency mice model. The maternal vitamin D deficiency (VDD) mice models and normal vitamin D status (CON) were successfully established by administering a vitamin D-free or vitamin D-sufficient diet for 4 weeks prior to pregnancy. The overall incidence of CAKUT was significantly increased in VDD neonatal mice (19.4% vs. 2.44%;

Indexed as

Glial Cell Line-Derived Neurotrophic FactorKidneyMAP Kinase Signaling SystemProto-Oncogene Proteins c-retVitamin D DeficiencyAnimalsDisease Models, AnimalFemaleMiceMitogen-Activated Protein Kinase 3PregnancySignal TransductionVitamin DGdnf protein, mouseGlial Cell Line-Derived Neurotrophic FactorMitogen-Activated Protein Kinase 3Proto-Oncogene Proteins c-retVitamin Dcongenital anomalies of the kidney and urinary tract (CAKUT)Gdnf-Ret-p-Erk1/2maternal vitamin D deficiency

Identifiers

PMID41977230
PMCPMC13073290

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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.