(Q33988143)

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Genome-wide gene expression analysis suggests an important role of hypoxia in the pathogenesis of endemic osteochondropathy Kashin-Beck disease

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Europe PubMed Central

PubMed publication ID

30 July 2017

Genome-wide gene expression analysis suggests an important role of hypoxia in the pathogenesis of endemic osteochondropathy Kashin-Beck disease (English)

1 reference

Europe PubMed Central

PubMed publication ID

30 July 2017

Kashin–Beck disease

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osteochondropathy

1 reference

based on heuristic

inferred from title

2

object named as

Xiong Guo

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Europe PubMed Central

PubMed publication ID

30 July 2017

object named as

Hua Yan

4

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author name string

Feng Zhang

1

1 reference

Europe PubMed Central

PubMed publication ID

30 July 2017

Weizhuo Wang

3

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Europe PubMed Central

PubMed publication ID

30 July 2017

Chunyan Li

5

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Europe PubMed Central

PubMed publication ID

30 July 2017

language of work or name

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publication date

29 July 2011

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Europe PubMed Central

PubMed publication ID

30 July 2017

1 reference

Europe PubMed Central

PubMed publication ID

30 July 2017

6

1 reference

Europe PubMed Central

PubMed publication ID

30 July 2017

7

1 reference

Europe PubMed Central

PubMed publication ID

30 July 2017

e22983

1 reference

Europe PubMed Central

PubMed publication ID

30 July 2017

copyright license

Creative Commons Attribution 4.0 International

29 July 2011

1 reference

April 2022 Public Data File from Crossref

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0 references

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1 reference

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5 July 2018

Mitochondrial function is altered in articular chondrocytes of an endemic osteoarthritis, Kashin-Beck disease

1 reference

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5 July 2018

Osteo-chondroprogenitor-specific deletion of the selenocysteine tRNA gene, Trsp, leads to chondronecrosis and abnormal skeletal development: a putative model for Kashin-Beck disease

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BAX activation is initiated at a novel interaction site

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Selenium for preventing Kashin-Beck osteoarthropathy in children: a meta-analysis

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Hypoxia activates NADPH oxidase to increase [ROS]i and [Ca2+]i through the mitochondrial ROS-PKCepsilon signaling axis in pulmonary artery smooth muscle cells.

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Hypoxia and osteoarthritis: how chondrocytes survive hypoxic environments

1 reference

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5 July 2018

Abnormal expression of Col X, PTHrP, TGF-beta, bFGF, and VEGF in cartilage with Kashin-Beck disease

1 reference

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The role of HIF-1alpha in maintaining cartilage homeostasis and during the pathogenesis of osteoarthritis

1 reference

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Gene set enrichment analysis: a knowledge-based approach for interpreting genome-wide expression profiles

1 reference

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Reactive oxygen species promote TNFalpha-induced death and sustained JNK activation by inhibiting MAP kinase phosphatases

1 reference

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Role of JNK activation in apoptosis: a double-edged sword

1 reference

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BCL-2, BCL-X(L) sequester BH3 domain-only molecules preventing BAX- and BAK-mediated mitochondrial apoptosis

1 reference

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Effects of physical therapy on patients with Kashin-Beck disease in Tibet

1 reference

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5 July 2018

Selenium, iodine and fungal contamination in Yulin District (People's Republic of China) endemic for Kashin-Beck disease

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3146522

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Epidemiological support for a multifactorial aetiology of Kashin-Beck disease in Tibet

1 reference

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Proapoptotic BAX and BAK: a requisite gateway to mitochondrial dysfunction and death

1 reference

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5 July 2018

Role of reactive oxygen species (ROS) in apoptosis induction

1 reference

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5 July 2018

Mitochondrial oxidative phosphorylation is a downstream regulator of nitric oxide effects on chondrocyte matrix synthesis and mineralization

1 reference

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The role of humic substances in drinking water in Kashin-Beck disease in China

1 reference

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5 July 2018

Kashin-Beck osteoarthropathy in rural Tibet in relation to selenium and iodine status

1 reference

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5 July 2018

Mitochondrial reactive oxygen species trigger hypoxia-induced transcription

1 reference

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Mitochondria and apoptosis

1 reference

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Study on the pathogenic factors of Kashin-Beck disease

1 reference

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Comparative analysis of gene expression profiles between primary knee osteoarthritis and an osteoarthritis endemic to Northwestern China, Kashin-Beck disease

1 reference

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GSEA-P: a desktop application for Gene Set Enrichment Analysis.

1 reference

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Reproducible genetic associations between candidate genes and clinical knee osteoarthritis in men and women.

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Hypoxia potentiates nitric oxide-mediated apoptosis in endothelial cells via peroxynitrite-induced activation of mitochondria-dependent and -independent pathways.

1 reference

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21 January 2018

Selenoprotein P gene r25191g/a polymorphism and quantification of selenoprotein P mRNA level in patients with Kashin-Beck disease.

1 reference

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21 January 2018

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Oxidative injury induced by synthetic humic acid polymer and monomer in cultured rabbit articular chondrocytes.

1 reference

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Fungal contamination in barley and Kashin-Beck disease in Tibet

1 reference

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Kashin-Beck disease

1 reference

https://api.crossref.org/works/10.1371%2FJOURNAL.PONE.0022983

21 January 2018

Chondrocyte apoptosis and expression of Bcl-2, Bax, Fas, and iNOS in articular cartilage in patients with Kashin-Beck disease.

1 reference

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29 October 2018

Association between polymorphism in DVWA and IL-1beta and Kashin-Beck disease

1 reference

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1 reference

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Oxidative stress induced by humic acid solvent extraction fraction in cultured rabbit articular chondrocytes

1 reference

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12 December 2020

based on heuristic

inferred from PubMed ID database lookup

Identifiers

10.1371/JOURNAL.PONE.0022983

1 reference

Europe PubMed Central

PubMed publication ID

30 July 2017

2011PLoSO...622983Z

0 references

PMC publication ID

1 reference

Europe PubMed Central

PubMed publication ID

30 July 2017

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

30 July 2017

ResearchGate publication ID

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