Evidence map›Paper›PMID 32591934›Full record

ArticleBiological trace element research2021

Decreased Expression of Heat Shock Protein 47 Is Associated with T-2 Toxin and Low Selenium-Induced Matrix Degradation in Cartilages of Kashin-Beck Disease.

Meng Zhang, Mengying Wang, Hui Wang, Ying Zhang, Zhengzheng Li, Yiping Feng, Yinan Liu, Yue Liu, Yucheng Liao, Wenjun Wang and 2 more

Abstract read
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In one paragraph

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 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

9 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
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  5. ER-resident proteins are key players in cartilage and bone homeostasis.Frontiers in cell and developmental biology · 2025
    Review
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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

12 authors at 1 institution in 1 country.

Meng Zhang *School of Public Health, Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases in National Health Commission of PR of China, Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Mengying Wang *School of Public Health, Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases in National Health Commission of PR of China, Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Hui WangSchool of Public Health, Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases in National Health Commission of PR of China, Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Ying ZhangSchool of Public Health, Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases in National Health Commission of PR of China, Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Zhengzheng LiSchool of Public Health, Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases in National Health Commission of PR of China, Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Yiping FengSchool of Public Health, Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases in National Health Commission of PR of China, Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Yinan LiuSchool of Public Health, Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases in National Health Commission of PR of China, Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Yue LiuSchool of Public Health, Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases in National Health Commission of PR of China, Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Yucheng LiaoSchool of Public Health, Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases in National Health Commission of PR of China, Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Wenjun WangSchool of Public Health, Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases in National Health Commission of PR of China, Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Qian FangSchool of Public Health, Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases in National Health Commission of PR of China, Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Jinghong ChenSchool of Public Health, Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases in National Health Commission of PR of China, Xi'an Jiaotong University, Xi'an, Shaanxi, China. chenjh.123@mail.xjtu.edu.cn.ORCID http://orcid.org/0000-0001-6819-4858
National Health and Family Planning Commission · CN

Funding

National Natural Science Foundation of China 81273006National Natural Science Foundation of China 81573102National Natural Science Foundation of China 81872565
6 · The paper itself

Abstract

Recent evidence suggests a role of type II collagen in Kashin-Beck disease (KBD) degeneration. We aimed to assess the abnormal expression of heat shock protein 47 (HSP47) which is associated with a decrease in type II collagen and an increase in cartilage degradation in KBD. Hand phalange cartilages were collected from KBD and healthy children. Rats were administered with T-2 toxin under the selenium (Se)-deficient diet. ATDC5 cells were seeded on bone matrix gelatin to construct engineered cartilaginous tissue. C28/I2 and ATDC5 cells and engineered tissue were exposed to different concentrations of T-2 toxin with or without Se. Cartilage degeneration was determined through histological evaluation. The distribution and expression of type II collagen and HSP47 were investigated through immunohistochemistry, western blotting, and real-time PCR. KBD cartilages showed increased chondronecrosis and extracellular matrix degradation in deep zone with decreased type II collagen and HSP47 expression. The low-Se + T-2 toxin animal group showed a significantly lower type II collagen expression along with decreased HSP47 expression. Decreased type II collagen and HSP47 in C28/I2 and ATDC5 cells induced by T-2 toxin showed a dose-dependent manner. Hyaline-like cartilage with zonal layers was developed in engineered cartilaginous tissues, with decreased type II collagen and HSP47 expression found in T-2 toxin-treated group. Se-supplementation partially antagonized the inhibitory effects of T-2 toxin in chondrocytes and cartilages. HSP47 plays a role in the degenerative changes of KBD and associated with T-2 toxin-induced decreased type II collagen expression, further promoting matrix degradation.

Indexed as

Cartilage, ArticularKashin-Beck DiseaseSeleniumT-2 ToxinAnimalsChondrocytesDisease Models, AnimalHSP47 Heat-Shock ProteinsRatsHSP47 Heat-Shock ProteinsSeleniumT-2 ToxinHeat shock protein 47Kashin-Beck diseaseMatrix degradationSeleniumT-2 toxinType II collagen

Identifiers

PMID32591934
OpenAlexW3037364629

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.