ArticleMammalian genome : official journal of the International Mammalian Genome Society2022
Mechanism of CREB1 in cardiac function of rats with heart failure via regulating the microRNA-376a-3p/TRAF6 axis.
Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 10 citations in OpenAlex.
- "Comprehensive multi-omics of age-respective plasma and matrix-bound extracellular vesicles identifies anti-fibrotic miRNAs validated on a heart-on-a-chip".Biomaterials · 2026Article
- Xinshuaining preparation ameliorates doxorubicin-induced cardiac injury in heart failure rats by regulating gut microbiota.Drug delivery and translational research · 2026Article
- CREB1 Silencing Protects Against Inflammatory Response in Rats with Deep Vein Thrombosis Through Reducing RPL9 Expression and Blocking NF-κB Signaling.Journal of cardiovascular translational research · 2024Article
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2 authors at 1 institution in 1 country.
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Abstract
Heart failure (HF) is a complicated disease resulting from impaired heart function. CREB1 is a candidate target in heart-concerning diseases. This paper attempts to explore the role of CREB1 in HF. Initially, the HF rat model was established by constricted abdominal aortic surgery and the cardiac function of HF rats was assessed by ultrasonic cardiogram. Levels of CK-MB and LDH and activity of Caspase-3 and Caspase-9 in HF rats were determined. Subsequently, myocardium pathological injury and myocardium apoptosis were detected. Additionally, the interactions between CREB1 and miR-376a-3p and between miR-376a-3p and TRAF6 were verified. The roles of CREB1, miR-376a-3p, and TRAF6 in HF were evaluated. In HF rats, CREB1 and miR-376a-3p were both downregulated while TRAF6 was upregulated. Besides, HF rats had decreased values of EF and FS, elevated levels of CK-MB and LDH, inflammatory infiltration, promoted cardiomyocyte apoptosis, and elevated activity of Caspase-3 and Caspase-9, which were all reversed by CREB1. Additionally, CREB1 activated miR-376a-3p expression, and miR-376a-3p targeted TRAF6 transcription. Both miR-376a-3p knockdown and TRAF6 overexpression annulled the protective role of CREB1 overexpression in cardiac function of HF rats. CREB1 activated miR-376a-3p expression to suppress TRAF6, thereby promoting the cardiac function of HF rats.
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