ArticleCanadian respiratory journal2020
Upregulation of Potassium Voltage-Gated Channel Subfamily J Member 2 Levels in the Lungs of Patients with Idiopathic Pulmonary Fibrosis.
Article in Canadian respiratory journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Identification and functional characterization of glycosyltransferase-related biomarkers for tuberculosis diagnosis.AMB Express · 2025Article
- Developing an IPF Prognostic Model and Screening for Key Genes Based on Cold Exposure-Related Genes Using Bioinformatics Approaches.Biomedicines · 2025Article
- Extravillous trophoblasts reverse the decidualization induced increase in matrix production by secreting TGFβ antagonists Emilin-1 and Gremlin-1.Cells & development · 2025Article
- Review
- Discrimination between NSIP- and IPF-Derived Fibroblasts Based on Multi-Parameter Characterization of Their Growth, Morphology and Physic-Chemical Properties.International journal of molecular sciences · 2022Article
- A transcriptomics-based meta-analysis identifies a cross-tissue signature for sarcoidosis.Frontiers in medicine · 2022Article
- The Optimization and Biological Significance of a 29-Host-Immune-mRNA Panel for the Diagnosis of Acute Infections and Sepsis.Journal of personalized medicine · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Fibroblast dysfunction is the main pathogenic mechanism underpinning idiopathic pulmonary fibrosis (IPF). Potassium voltage-gated channel subfamily J member 2 (KCNJ2) plays critical roles in the proliferation of myofibroblasts and in the development of cardiac fibrosis. Objectives: This study aimed to evaluate the role of KCNJ2 in IPF. Methods: Results: Conclusion: KCNJ2 may participate in the development of IPF, and its protein level may be a candidate diagnostic and therapeutic molecule for IPF.
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Registered trials
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