ArticleExperimental and therapeutic medicine2022
lncRNA HOTAIR mediates OGD/R-induced cell injury and angiogenesis in a EZH2-dependent manner.
Article in Experimental and therapeutic medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- LncRNA HOTAIR/miR-9-5p/FOXP1 axis modulates cerebral ischemia-reperfusion injury via NLRP3 inflammasome activation.IBRO neuroscience reports · 2026Article
- GPR75 mediates hyperuricemia-induced endothelial inflammatory injury via a HOTAIR/miR-141-3p regulatory network.Molecular biology reports · 2026Article
- Silencing of lncRNA HOTAIR Using Eyedrops as a Potential Treatment for Diabetes-Associated Retinal Dysregulation and Dysfunction.Investigative ophthalmology & visual science · 2026Article
- Catechins in stroke: multi-target mechanisms, preclinical evidence, and translational challenges.Frontiers in pharmacology · 2026Review
- Unveiling the Role of LncRNA in Sepsis-Associated Encephalopathy.Current medical science · 2025Review
- Unlocking the therapeutic potential of tumor-derived EVs in ischemia-reperfusion: a breakthrough perspective from glioma and stroke.Journal of neuroinflammation · 2025Review
- LncRNAs Orchestrating Neuroinflammation: A Comprehensive Review.Cellular and molecular neurobiology · 2025Review
- Ischemic Stroke and the Biological Hallmarks of Aging.Aging and disease · 2024Review
- The multifaceted functions of long non-coding RNAExpert reviews in molecular medicine · 2024Review
- Roles of HOTAIR Long Non-coding RNA in Gliomas and Other CNS Disorders.Cellular and molecular neurobiology · 2024Review
- Analysis and Regulatory Mechanisms of Platelet-Related Genes in Patients with Ischemic Stroke.Cellular and molecular neurobiology · 2024Article
- Spotlight on HOX cluster‑embedded antisense lncRNAs in cardiovascular diseases (Review).International journal of molecular medicine · 2023Review
- LncRNAs and CircRNAs as Strategies against Pathological Conditions Caused by a Hypoxic/Anoxic State.Biomolecules · 2023Review
- Epigenetic mechanisms and potential therapeutic targets in stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022Review
- Effects of ischemic postconditioning and long non-coding RNAs in ischemic stroke.Bioengineered · 2022Review
- Experimental Models for Testing the Efficacy of Pharmacological Treatments for Neonatal Hypoxic-Ischemic Encephalopathy.Biomedicines · 2022Review
- Long Non-coding RNA HOTAIR in Central Nervous System Disorders: New Insights in Pathogenesis, Diagnosis, and Therapeutic Potential.Frontiers in molecular neuroscience · 2022Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non-coding RNAs (lncRNA) serve an important role in neonatal hypoxic-ischemic encephalopathy (HIE) have been reported to regulate the activity of HIE-associated proteins. The present study aimed to elucidate the role of Hox transcript antisense intergenic RNA (HOTAIR) in oxygen-glucose deprivation/reperfusion (OGD/R)-induced injury in human brain microvascular endothelial cells (hBMVECs). The levels of HOTAIR were evaluated in the serum of neonatal patients with HIE, and the effects of HOTAIR were evaluated using
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.