ArticleGenes & genomics2019
Long noncoding RNA UCA1 inhibits ischaemia/reperfusion injury induced cardiomyocytes apoptosis via suppression of endoplasmic reticulum stress.
Article in Genes & genomics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 30 citations in OpenAlex.
- Article
- The role of UPR-related long noncoding RNAs in development of endocrine resistance in breast cancer.International journal of cancer · 2025Review
- LncRNA UCA1 enhances NRF2 expression through the mJournal of bioenergetics and biomembranes · 2024Article
- Upregulation of LncRNA UCA1 promotes cardiomyocyte proliferation by inhibiting the miR-128/SUZ12/P27 pathway.Heliyon · 2024Article
- Endoplasmic reticulum stress signaling modulates ischemia/reperfusion injury in the aged heart by regulating mitochondrial maintenance.Molecular medicine (Cambridge, Mass.) · 2024Review
- LncRNAs and CircRNAs in Endoplasmic Reticulum Stress: A Promising Target for Cardiovascular Disease?International journal of molecular sciences · 2023Review
- Non-coding RNA mediates endoplasmic reticulum stress-induced apoptosis in heart disease.Heliyon · 2023Review
- Non-coding RNAs in human health and disease: potential function as biomarkers and therapeutic targets.Functional & integrative genomics · 2023Review
- Regulators of epigenetic change in ferroptosis‑associated cancer (Review).Oncology reports · 2022Review
- Review
- Review
- Oxidative Stress and Inflammation in Cardiovascular Diseases and Cancer: Role of Non-coding RNAs.The Yale journal of biology and medicine · 2022Review
- Mitochondrial Dysfunction in Cardiovascular Diseases: Potential Targets for Treatment.Frontiers in cell and developmental biology · 2022Review
- Noncoding RNAs: biology and applications-a Keystone Symposia report.Annals of the New York Academy of Sciences · 2021Review
- Long Non-Coding RNAs in Cardiovascular Diseases: Potential Function as Biomarkers and Therapeutic Targets of Exercise Training.Non-coding RNA · 2021Review
- Article
- Urothelial Cancer Associated 1 (UCA1) and miR-193 Are Two Non-coding RNAs Involved in Trophoblast Fusion and Placental Diseases.Frontiers in cell and developmental biology · 2021Article
- The Role of Long Non-coding RNAs in Sepsis-Induced Cardiac Dysfunction.Frontiers in cardiovascular medicine · 2021Review
- LncRNA A2M-AS1 lessens the injury of cardiomyocytes caused by hypoxia and reoxygenation via regulating IL1R2.Genes & genomics · 2020Article
- Endoplasmic reticulum stress serves an important role in cardiac ischemia/reperfusion injury (Review).Experimental and therapeutic medicine · 2020Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIschemia heart disease is one of the major causes of death worldwide which often associated with tissue infarction and limit the recovery of function. Multiple factors involved in the I/R-induced cardiomyocyte dysfunction which were consistent with a role of oxidative stress and altered endothelium-dependent responses. However, the pathogenic mechanisms in I/R injury remain unclear. MATERIALS AND
methodsThe H9C2 cells were in the ischaemia/reperfusion (I/R) condition. After I/R, the cells were transfected with or without adenovirus-urothelial carcinoma associated 1(Ad-UCA1). Then qRT-PCR analysis was performed to quantify mRNA expression of different treatment groups. Cell apoptosis rate was assessed using flow cytometry and ER stress biomarker expression were measured by immunoblotting. Intracellular and mitochondrial ROS generation were assayed by fluorescence microscope after staining with the DCFDA or MitoSOX.
resultsI/R conditions trigger lncRNAs UCA1 expression, cellular and mitochondria ROS production, resulting in cell apoptosis through the induction of oxidative and ER stress. Overexpression of UCA1 protects H9C2 cells from I/R-induced ER stress and cell apoptosis. Moreover, UCA1 might be a potential regulator in the protective effect of I/R‑induced oxidative stress and mitochondria dysfunction. Subsequently, ER stress inhibitor attenuated the effect of siUCA1 induced injury in H9C2 cells.
conclusionThe expression of UCA1 against I/R induced oxidative stress and mitochondria dysfunction via suppression of endoplasmic reticulum stress. UCA1 might be a biomarker to improved diagnosis of I/R injury.
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