ArticleBioengineered2021
Argon inhibits reactive oxygen species oxidative stress via the miR-21-mediated PDCD4/PTEN pathway to prevent myocardial ischemia/reperfusion injury.
Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Effect of adjuvant therapy with compound danshen drip pill on inflammatory factors and cardiac function after percutaneous coronary intervention for acute myocardial infarction: a systematic review and meta-analysis.Frontiers in pharmacology · 2024Pooled it
- Programmed cell death protein 4 (PDCD4): a pleiotropic regulator in cardiovascular diseases.Journal of physiology and biochemistry · 2026Review
- EV-Encapsulated Mitochondrial miRNAs: Enhancing Cardiomyocyte Bioenergetics.International journal of molecular sciences · 2026Review
- Therapeutic Effects of Argon Inhalation on Lung Ischemia-Reperfusion Injury in CLAWN Miniature Swine.Journal of clinical medicine · 2025Article
- Virus-Induced MicroRNA Modulation and Systemic Sclerosis Disease.Biomedicines · 2024Review
- Association of endometriosis with Sjögren's syndrome: Genetic insights (Review).International journal of molecular medicine · 2024Review
- Effect of zearalenone on the jejunum of weaned gilts through the Epac1/Rap1/JNK pathway.Journal of animal science · 2024Article
- Article
- Oxidative Stress and Epigenetics: miRNA Involvement in Rare Autoimmune Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- Hematoporphyrin monomethyl ether mediated photodynamic therapy inhibits oral squamous cell carcinoma by regulating the P53-miR-21-PDCD4 axis via singlet oxygen.Lasers in medical science · 2022Article
- IFC-305 attenuates renal ischemia-reperfusion injury by promoting the production of hydrogen sulfide (HBioengineered · 2022Article
- Article
- The anti-fibrotic agent nintedanib protects chondrocytes against tumor necrosis factor-ɑ (TNF-ɑ)-induced extracellular matrix degradation.Bioengineered · 2022Article
- Circular RNA Rbms1 inhibited the development of myocardial ischemia reperfusion injury by regulating miR-92a/BCL2L11 signaling pathway.Bioengineered · 2022Article
- The mir-21 Inhibition Enhanced HUVEC Cellular Viability during Hypoxia-Reoxygenation Injury by Regulating PDCD4.Mediators of inflammation · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The objective of this study was to explore the effect of argon preconditioning on myocardial ischemia reperfusion (MI/R) injury and its mechanism. Cardiomyocytes H2C9 were pre-treated with 50% argon, and a cell model of oxygen-glucose deprivation (OGD) was established. CCK-8 and cytotoxicity detection kits were used to detect cell viability and lactate dehydrogenase (LDH) release. The miR-21 expression was detected using quantitative real-time polymerase chain reaction. Western blot analysis was performed to detect the expression of programmed cell death protein 4 (PDCD4) and homologous phosphatase and tensin homolog (PTEN) proteins. The levels of inflammatory factors (IL-1β, IL-6, and IL-8) and oxidative stress factors (reactive oxygen species ROS], malondialdehyde [MDA], and superoxide dismutase [SOD]) were measured using an enzyme-linked immunosorbent assay. The effect of argon on cell apoptosis was detected using flow cytometry. Argon increased the proliferation of cardiomyocytes induced by OGD, decreased the release of LDH in cell culture medium, increased miR-21 expression in cells, decreased the expression of miR-21 target proteins PDCD4 and PTEN, decreased the levels of inflammatory factors (interleukin-1β [IL-1β], interleukin-6 [IL-6], and interleukin-8 [IL-8]) and oxidative stress factors (ROS and MDA), increased the SOD content, and decreased the cell apoptosis rate. Our results suggest that argon preconditioning inhibited the PDCD4/PTEN pathway via miR-21, thereby inhibiting ROS oxidative stress and preventing MI/R injury.
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