ArticleJournal of cellular physiology2019
microRNA-665 silencing improves cardiac function in rats with heart failure through activation of the cAMP signaling pathway.
Article in Journal of cellular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.
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Who cites it
17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 29 citations in OpenAlex.
- Noncoding RNA as potential therapeutics to rescue mitochondrial dysfunction in cardiovascular diseases.American journal of physiology. Heart and circulatory physiology · 2025Pooled it
- A meta-analysis of microRNA expression profiling studies in heart failure.Heart failure reviews · 2021Pooled it
- Higher circulating ACE2 and DPP3 but reduced ACE and angiotensinogen in hyperreninemic sepsis patients.Clinical science (London, England : 1979) · 2025Article
- Integrated gene expression profiles reveal a transcriptomic network underlying the thermogenic response in adipose tissue.Scientific reports · 2023Article
- Article
- Hsa_circ_0003748 promotes disease progression in rheumatic valvular heart disease by sponging miR-577.Journal of clinical laboratory analysis · 2022Article
- MicroRNA-665-3p exacerbates nonalcoholic fatty liver disease in mice.Bioengineered · 2022Article
- Hypoxic/Ischemic Inflammation, MicroRNAs and δ-Opioid Receptors: Hypoxia/Ischemia-Sensitive Versus-Insensitive Organs.Frontiers in aging neuroscience · 2022Review
- Inflammation and Oxidative Stress in Diabetic Kidney Disease: The Targets for SGLT2 Inhibitors and GLP-1 Receptor Agonists.International journal of molecular sciences · 2021Review
- Mitochondrial nucleoid in cardiac homeostasis: bidirectional signaling of mitochondria and nucleus in cardiac diseases.Basic research in cardiology · 2021Review
- Characterization of CB2 Receptor Expression in Peripheral Blood Monocytes of Acute Ischemic Stroke Patients.Translational stroke research · 2021Article
- microRNA-454-mediated NEDD4-2/TrkA/cAMP axis in heart failure: Mechanisms and cardioprotective implications.Journal of cellular and molecular medicine · 2021Article
- MicroRNAs Regulating Mitochondrial Function in Cardiac Diseases.Frontiers in pharmacology · 2021Review
- MiR-665 Regulates Vascular Smooth Muscle Cell Senescence by Interacting With LncRNA GAS5/SDC1.Frontiers in cell and developmental biology · 2021Article
- To Explore the Mechanism and Equivalent Molecular Group of Fuxin Mixture in Treating Heart Failure Based on Network Pharmacology.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- MicroRNA Mediated Cardioprotection - Is There a Path to Clinical Translation?Frontiers in bioengineering and biotechnology · 2020Review
- MicroRNA-665 mediates propofol-induced cell apoptosis in human stem cell-derived neurons.Bioengineered · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heart failure (HF) is a disease with high mortality and morbidity rate. Previous studies have shown that microRNAs (miRNAs) may be implicated in the pathogenesis of HF, potentially being able to improve the cardiac function in an HF rat model. The present study was designed to define the role of miR-665 in the cardiac function of the HF rats. Following the establishm;ent of the rat models of HF, the functional role miR-665 in HF was determined using an ectopic expression and knockdown experiments. The cardiac function was evaluated with the determination of ventricular mass index and hemodynamic parameters. Terminal deoxynucleotidyl transferase dUTP nick end labeling staining was performed, with the apoptosis of cardiac cells detected in the process. The expression of miR-665, glucagon-like peptide 1 receptor (GLP1R), cyclic adenosine monophosphate (cAMP) signaling pathway-related, and apoptosis-related genes was examined. Enzyme-linked immunosorbent assay was conducted to determine the levels of inflammation-related genes. Initially, the upregulation of miR-665, downregulation of GLP1R, and inactivation of cAMP signaling pathway were observed in HF rats. GLP1R was a target of miR-665. Forced expression of miR-665 promoted cell apoptosis and inhibited GLP1R and the cAMP signaling pathway. In addition, miR-665 overexpression has been known to impair cardiac function, promote inflammatory response while elevating malondialdehyde and superoxide dismutase levels, and decreasing mitochondrial respiratory chain enzyme activities. Furthermore, we also observed that the effects of miR-665 inhibition had been reversed when the cAMP signaling pathway was also inhibited. This study demonstrates that miR-665 inhibition can stabilize the cardiac function of HF rats via the cAMP signaling pathway via upregulation of the GLP1R.
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