ArticleESC heart failure2022
Knockdown of XIST up-regulates 263294miR-340-5p to relieve myocardial ischaemia-reperfusion injury via inhibiting cyclin D1.
Article in ESC heart failure, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Review
- RNA-Based Biomarkers for Diagnostic Discrimination of Ischemic and Hemorrhagic Stroke: A Systematic Review.Journal of clinical medicine · 2026Review
- Integrative transcriptomic and single-cell analysis reveals mitochondrial-related gene biomarkers in heart failure with preserved ejection fraction.Scientific reports · 2025Article
- Mitochondrial dysfunction in AMI: mechanisms and therapeutic perspectives.Journal of translational medicine · 2025Review
- LncRNA XIST: A Breakthrough in Inflammation-related Diseases.Current medicinal chemistry · 2025Review
- GTF2E2 downregulated by miR-340-5p inhibits the malignant progression of glioblastoma.Cancer gene therapy · 2023Article
- miR-1183 Is a Key Marker of Remodeling upon Stretch and Tachycardia in Human Myocardium.International journal of molecular sciences · 2022Article
- Knockdown of XIST up-regulates 263294miR-340-5p to relieve myocardial ischaemia-reperfusion injury via inhibiting cyclin D1.ESC heart failure · 2022Article
- miR-340-5p Alleviates Oxidative Stress Injury by Targeting MyD88 in Sepsis-Induced Cardiomyopathy.Oxidative medicine and cellular longevity · 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
aimLong non-coding RNAs (lncRNAs) are known to participate in various human diseases, while the role of X inactive-specific transcript (XIST) binding microRNA-340-5p (miR-340-5p) remains seldom studied. We aim to identify the role of the XIST/miR-340-5p/cyclin D1 (CCND1) axis in the myocardial ischaemia-reperfusion injury (MIRI). METHODS AND
resultsThe mouse MIRI models were established. The expression of XIST, miR-340-5p, and CCND1 in mouse myocardial tissues in MIRI mice was assessed. The MIRI mice were respectively treated with altered XIST, miR-340-5p, or CCND1. The changes of myocardial enzyme activity were assessed, and the cardiac function was evaluated. Myocardial pathological changes, cardiomyocyte apoptosis and related apoptotic factors, oxidative stress and inflammatory factors were observed in myocardial tissues in mice with MIRI. The binding relationships between XIST and miR-340-5p, and between miR-340-5p and CCND1 were confirmed. XIST and CCND1 were up-regulated while miR-340-5p was down-regulated in MIRI mice. Silenced XIST could elevated miR-340-5p expression and reduced CCND1 expression, so as to promoted cardiac function and suppressed myocardial enzyme activity, ameliorated pathological changes, decelerated cardiomyocyte apoptosis by elevating Bcl-2 but reducing the levels of Bax and Caspase-3, attenuated inflammatory response by repressing IL-6 and TNF-α levels, and mitigated oxidative stress by reducing MDA contents and increasing CAT, GSH-Px, and SOD levels in MIRI mice. XIST sponged miR-340-5p and miR-340-5p targeted CCND1.
conclusionsKnockdown of XIST up-regulates miR-340-5p to relieve MIRI via inhibiting CCND1.
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