ArticleCytotechnology2021
NFKB1-mediated downregulation of microRNA-106a promotes oxidative stress injury and insulin resistance in mice with gestational hypertension.
Article in Cytotechnology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 8 citations in OpenAlex.
- Adaptive evolution at thyroid hormone, insulin and glycerolipid pathways improved energy metabolism in high-latitude Eurasian populations.Communications biology · 2026Article
- Enolase and 16.5-kDa Tegument-Associated Protein inJournal of extracellular biology · 2025Article
- Identifying Diagnostic Markers and Constructing Predictive Models for Oxidative Stress in Multiple Sclerosis.International journal of molecular sciences · 2024Article
- Deciphering NF-kappaB pathways in smoking-related lung carcinogenesis.EXCLI journal · 2024Review
- MiR-106a facilitates the sensorineural hearing loss induced by oxidative stress by targeting connexin-43.Bioengineered · 2022Article
- Intracranial Aneurysms Induced byFrontiers in neurology · 2022Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study intended to investigate the role of NFKB1 in oxidative stress injury and insulin resistance in gestational hypertension (GH) mice. Following establishment of a GH mouse model by high-fat diet, NFKB1, miR-106a, and FLOT2 expression was detected in liver of mice. After NFKB1, miR-106a, and FLOT2 were altered in GH mice by lentiviral vector, oxidative stress markers in liver tissues were examined by colorimetry, and insulin resistance was assessed by fasting blood glucose and fasting insulin levels. Next, hepatocytes were isolated from GH mice and treated with miR-106a mimic, inhibitor or siRNA, followed by determination of hepatocyte apoptosis and the expression of inflammation- and apoptosis-related factors. Evaluation of the correlations among NFKB1, miR-106a, and FLOT2 were conducted. Liver of GH mice harbored NFKB1 and FLOT2 upregulation and miR-106a downregulation. miR-106a was transcriptionally inhibited by NFKB1, and negatively targeted FLOT2. Oxidative stress injury and insulin resistance in GH mice and apoptosis and inflammation of hepatocytes from GH mice were decreased after silencing NFKB1 or FLOT2 or overexpressing miR-106a. These findings provided evidence demonstrating the inhibitory effect of NFKB1 silencing on oxidative stress injury and insulin resistance in GH mice via miR-106a upregulation and FLOT2 downregulation.
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Registered trials
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