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• W3048227908 abstract "Background: Chronic heart failure (CHF) is a major health burden worldwide, but there are a lack of effective methods for its early diagnosis and prognostic evaluation. Circular RNAs (circRNA), as a class, have been found to regulate gene expression and are implicated in multiple types of diseases. The circRNA, CDR1as, is reported to regulate gene transcription by acting as a microRNA inhibitor. However, the role of CDR1as in CHF remains to be elucidated. The aim of this study was to investigate the role and mechanism of action of the circRNA, CDR1as, in CHF. Methods: A total of 30 patients with CHF and 30 healthy persons were included in the study. The levels of CDR1as, miR-135a, and miR-135b in the plasma of all subjects were quantified by qRT-PCR. ELISA was used to detect the level of HMOX1 in plasma. The effect of CDR1as was investigated in human cardiomyocytes, including HCMs and AC16 cells. Results: CDR1as was upregulated in the plasma of patients with CHF and is a potential diagnostic marker of CHF. The levels of miR-135a and miR-135b were downregulated in the plasma of patients with CHF. The plasma level of HMOX1 in patients with CHF was significantly higher compared with the control group and was highly correlated with cardiac function in CHF patients. CDR1as was shown to act as a sponge for miR-135a and miR-135b and regulated the proliferation and apoptosis of human cardiomyocytes through the miR-135a/HMOX1 and miR-135b/HMOX1 signaling axes. Conclusion: CDR1as is a potential biomarker of CHF that is mechanistically involved in the disease pathogenesis and participates in regulating the occurrence and development of CHF through the miR-135a/HMOX1 and miR-135b/HMOX1 signaling axes." @default.
• W3048227908 created "2020-08-13" @default.
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• W3048227908 date "2020-09-01" @default.
• W3048227908 modified "2023-10-17" @default.
• W3048227908 title "The Circular RNA CDR1as Regulates the Proliferation and Apoptosis of Human Cardiomyocytes Through the miR-135a/HMOX1 and miR-135b/HMOX1 Axes" @default.
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• W3048227908 doi "https://doi.org/10.1089/gtmb.2020.0034" @default.
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