Evidence map›Paper›PMID 39775139›Full record

ArticleScientific reports2025

Histopathological effects of hypervitaminosis-D and the protective role of fetuin-A in renal, hepatic, and cardiac tissues in a murine model.

Maha A Mohamed, Mohamed Hussein, Shefaa Moustafa, Yalda Rahmani, Tooba Ahmed Durrani, Shiza Ali, Hafsa Ubaid Chhapra, Elshimaa Ali, Mariam Shadan

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
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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.

Maha A MohamedDepartment of Biomedical Sciences, Dubai Medical College for Girls, Muhaisanah-1, Dubai, UAE.
Mohamed HusseinDepartment of Biomedical Sciences, Dubai Medical College for Girls, Muhaisanah-1, Dubai, UAE.
Shefaa MoustafaDepartment of Biomedical Sciences, Dubai Medical College for Girls, Muhaisanah-1, Dubai, UAE.
Yalda RahmaniDepartment of Biomedical Sciences, Dubai Medical College for Girls, Muhaisanah-1, Dubai, UAE.
Tooba Ahmed DurraniDepartment of Biomedical Sciences, Dubai Medical College for Girls, Muhaisanah-1, Dubai, UAE.
Shiza AliDepartment of Biomedical Sciences, Dubai Medical College for Girls, Muhaisanah-1, Dubai, UAE.
Hafsa Ubaid ChhapraDepartment of Biomedical Sciences, Dubai Medical College for Girls, Muhaisanah-1, Dubai, UAE.
Elshimaa AliDepartment of Biomedical Sciences, Dubai Medical College for Girls, Muhaisanah-1, Dubai, UAE.
Mariam ShadanDepartment of Biomedical Sciences, Dubai Medical College for Girls, Muhaisanah-1, Dubai, UAE. dr.mariam@dmcg.edu.ORCID 0000-0002-9660-9149

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypervitaminosis D leads to toxic effects, including hypercalcemia, which can cause severe damage to various organs. Fetuin-A, a glycoprotein with anti-inflammatory properties, may protect tissues from such damage. This study explores the role of Fetuin-A in mitigating hypervitaminosis D-induced damage in renal, hepatic, and cardiac tissues. The objectives of this study were to: (1) Assess the extent of tissue damage from high-dose vitamin D in a murine model by examining the histopathological changes in liver, kidney and heart. (2) Investigate Fetuin-A's protective effect against this damage. Thirty-six albino rats were divided into four groups: (1) control, (2) vitamin D toxicity, (3) Fetuin-A + vitamin D, and (4) Fetuin-A only. Vitamin D was administered subcutaneously at 250 μg/20 g/day for 3 days. Fetuin-A was given at 100 μl/20 g, starting 7 days before vitamin D treatment. Histopathological analysis of liver, kidney, and heart tissues was performed using H&E and Alizarin Red staining and findings were analysed statistically. Vitamin D toxicity caused significant tissue damage, including apoptosis, inflammation, and calcification in the liver, kidneys, and heart. Pre-treatment with Fetuin-A reduced calcification and inflammation, preserving tissue architecture. Fetuin-A-only rats showed no damage or calcification. Fetuin-A provided statistically significant protection against vitamin D-induced damage, reducing oxidative stress and calcification in affected organs. These findings suggest Fetuin-A could be a potential therapeutic agent for hypervitaminosis D.

Indexed as

alpha-2-HS-GlycoproteinDisease Models, AnimalKidneyLiverMyocardiumVitamin DAnimalsApoptosisCalcinosisHeartMaleMiceOxidative StressRatsalpha-2-HS-GlycoproteinVitamin DCalcificationFetuin-AHypervitaminosis DTissue damageVitamin D toxicity

Identifiers

PMID39775139
PMCPMC11706989

What Socratic holds

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LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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 Socratic graph.