ArticleBioengineered2022
Dexmedetomidine protects H9C2 rat cardiomyocytes against hypoxia/reoxygenation injury by regulating the long non-coding RNA colon cancer-associated transcript 1/microRNA-8063/Wnt/β-catenin axis.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 3 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.
The trial behind it
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
3 citing papers in PubMed, 9 citations in OpenAlex.
- Insight into Cardioprotective Effects and Mechanisms of Dexmedetomidine.Cardiovascular drugs and therapy · 2024Review
- Dexmedetomidine ameliorates diabetic intestinal injury by promoting the polarization of M2 macrophages through the MMP23B pathway.World journal of diabetes · 2024Article
- Dexmedetomidine ameliorates x-ray-induced myocardial injury via alleviating cardiomyocyte apoptosis and autophagy.BMC cardiovascular disorders · 2024Article
Corrections and comments
- Retracted
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dexmedetomidine (Dex) protects the heart from ischemia/reperfusion (I/R) injury. The differential expression of long non-coding RNAs (lncRNAs) is associated with myocardial injury, but whether the lncRNA colon cancer-associated transcript 1 (CCAT1) is associated with Dex-mediated myocardial protection remains unclear. In this study, a hypoxia/reoxygenation (H/R) H9C2 model was established to simulate the in vitro characteristics of I/R. CCAT1 and microRNA (miR)-8063 expression levels in H/R H9C2 cells pretreated with Dex were determined via quantitative reverse transcription-polymerase chain reaction. The survival and apoptotic rates of H9C2 cells were determined via cell counting kit-8 and flow cytometry assays. Wnt3a, Wnt5a, and β-catenin protein levels were measured via western blotting. Luciferase and RNA immunoprecipitation assays were used to explore the binding relationship between miR-8063 and CCAT1. Dex pretreatment increased H/R H9C2 cell viability and CCAT1 expression, while decreasing the cell apoptosis and Wnt3a, Wnt5a, and β-catenin protein levels. Knockdown of CCAT1 abolished the protective effects of Dex on H/R H9C2 cells, and the downregulation of miR-8063 expression eliminated the effect of CCAT1 knockdown. These results revealed that CCAT1, a sponge for miR-8063, is involved in Dex-mediated H9C2 cell H/R injury by negatively targeting miR-8063 and inactivating the Wnt/β-catenin pathway. Dex protects H9C2 cells from H/R impairment by regulating the lncRNA CCAT1/miR-8063/Wnt/β-catenin axis.
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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 OpenQuestion graph.