Evidence map›Paper›PMID 32172502›Full record

ArticleBiological trace element research2021

Selenium Deficiency-Induced Damage and Altered Expression of Mitochondrial Biogenesis Markers in the Kidneys of Mice.

Hehuan Lai, Tingting Nie, Yitong Zhang, Ying Chen, Jiaqi Tao, Tingting Lin, Tangdong Ge, Fenglan Li, Hui Li

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Article in Biological trace element research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

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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

Who cites it

22 citing papers in PubMed, 40 citations in OpenAlex.

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  5. Nutritional and Therapeutic Potential ofJournal of fungi (Basel, Switzerland) · 2025
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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 at 1 institution in 1 country.

Hehuan LaiDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Baojian Road 157, Nangang District, Harbin City, 150081, Heilongjiang Province, China.
Tingting NieDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Baojian Road 157, Nangang District, Harbin City, 150081, Heilongjiang Province, China.
Yitong ZhangDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Baojian Road 157, Nangang District, Harbin City, 150081, Heilongjiang Province, China.
Ying ChenDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Baojian Road 157, Nangang District, Harbin City, 150081, Heilongjiang Province, China.
Jiaqi TaoDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Baojian Road 157, Nangang District, Harbin City, 150081, Heilongjiang Province, China.
Tingting LinDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Baojian Road 157, Nangang District, Harbin City, 150081, Heilongjiang Province, China.
Tangdong GeDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Baojian Road 157, Nangang District, Harbin City, 150081, Heilongjiang Province, China.
Fenglan LiDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Baojian Road 157, Nangang District, Harbin City, 150081, Heilongjiang Province, China.
Hui LiDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Baojian Road 157, Nangang District, Harbin City, 150081, Heilongjiang Province, China. lihui@ems.hrbmu.edu.cn.
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies have raised concerns that kidney disease is often closely related to low serum Se levels in patients and that hyposelenemia may increase the vulnerability of patients to complications. However, few studies examining renal injury caused by Se deficiency have been conducted. To determine the effects of a selenium-deficient diet on renal function, a mouse model was fed a selenium-deficient diet (0.02 mg Se/kg) for 20 weeks. Meanwhile, mice in the control group (selenium-adequate) were fed a standard diet (0.18 mg Se/kg). The cellular models were established by lentiviral Trnau1ap-shRNA vectors transfected into mouse podocyte (MPC5) and mouse renal tubular epithelial (TCMK1) cell lines. Significant increases in serum creatinine levels and urinary protein/creatinine ratios were accompanied by increased MDA content in the Se-deficient group compared to the control group. The morphological observations of tissues showed widespread inflammation and ultrastructural changes in the Se-deficient group, such as swollen mitochondria and extensive podocyte fusion and renal tubular microvilli shedding. In addition, the expression of COXIV and cytochrome c was significantly downregulated in the Se-deficient group. Importantly, the mRNA levels of silent mating type information regulation 2 homolog 1 (SIRT1) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and the protein levels of SIRT1 were increased in the Se-deficient group compared with the normal control group. Our data indicate that Se deficiency induces renal injury in mice. The elevated oxidative stress caused by Se deficiency may result in mitochondrial damage, which might affect renal function. Moreover, the SIRT1/PGC1α axis likely plays an important role in the compensatory mechanism of mitochondrial dysfunction.

Indexed as

Organelle BiogenesisSeleniumAnimalsHumansKidneyMiceMitochondriaPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaTranscription FactorsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaSeleniumTranscription FactorsMitochondrial biogenesisMitochondrial damageOxidative stressRenal injurySelenium deficiencySIRT1/PGC1α

Identifiers

PMID32172502
OpenAlexW3011848286

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.