{
    "abstract": "Diabetic cardiomyopathy (DCM) is a common cardiovascular disease. A declined miR-20a-5p was observed in hearts of diabetic mice, while its effect on DCM remains unknown. Herein, we established streptozotocin-induced DCM rat model and high glucose-stimulated H9C2 model of DCM. Then they were treated with adenovirus expressing miR-20a-5p to explore the function of miR-20a-5p. Insulin tolerance test and intraperitoneal glucose tolerance test assay revealed that miR-20a-5p reduced blood glucose level. Besides, miR-20a-5p improved cardiac dysfunction reflected by reduced heart weight/body weight and left ventricular diastolic pressure, and increased left ventricular systolic pressure and \u00b1LV dp/dt max. MiR-20a-5p prevented cardiomyocyte apoptosis, along with the upregulated c-caspase-3, bax and downregulated bcl-2. Moreover, miR-20a-5p alleviated cardiac hypertrophy as the parameters of atrial natriuretic peptide, B-type natriuretic peptide and MyHC-\u03b2 decreased. Also, miR-20a-5p attenuated the cardiac fibrosis demonstrated by decreased transforming growth factor-\u03b21, collagen I levels and the inflammatory response manifested by reduced interleukin-6, tumour necrosis factor-\u03b1 and IL-1\u03b2 production. Furthermore, miR-20a-5p prevented Jun NH2-terminal kinase (JNK) phosphorylation and nuclear factor-\u03baB (NF-\u03baB) p65nuclear translocation. Similarly, the effects of miR-20a-5p on DCM were confirmed in our in vitro experiments. Additionally, ROCK2 is a possible target gene of miR-20a-5p. ROCK2 overexpression reversed the protective effect of miR-20a-5p on DCM. Overall, miR-20a-5p may effectively ameliorate DCM through improving cardiac metabolism, and subsequently inhibiting inflammation, apoptosis, hypertrophy, fibrosis and JNK/NF-\u03baB pathway via modulating ROCK2.",
    "authors": [
        {
            "affiliation": "Department of Cardiology, The Second Hospital of Hebei Medical University, No. 215, Heping West Road, Shijiazhuang 050000, China.\nThe Third Department of Cardiology, Cangzhou Central Hospital, No.16, Xinhua West Road, Cangzhou 061000, China.",
            "firstname": "Xiaoyu",
            "initials": "X",
            "lastname": "Liu"
        },
        {
            "affiliation": "Department of Cardiology, The Second Hospital of Hebei Medical University, No. 215, Heping West Road, Shijiazhuang 050000, China.",
            "firstname": "Bingyan",
            "initials": "B",
            "lastname": "Guo"
        },
        {
            "affiliation": "The Third Department of Cardiology, Cangzhou Central Hospital, No.16, Xinhua West Road, Cangzhou 061000, China.",
            "firstname": "Wei",
            "initials": "W",
            "lastname": "Zhang"
        },
        {
            "affiliation": "The Third Department of Cardiology, Cangzhou Central Hospital, No.16, Xinhua West Road, Cangzhou 061000, China.",
            "firstname": "Bocong",
            "initials": "B",
            "lastname": "Ma"
        },
        {
            "affiliation": "Department of Cardiology, The Second Hospital of Hebei Medical University, No. 215, Heping West Road, Shijiazhuang 050000, China.",
            "firstname": "Yongjun",
            "initials": "Y",
            "lastname": "Li"
        }
    ],
    "conclusions": null,
    "copyrights": "\u00a9 The Author(s) 2021. Published by Oxford University Press on behalf of the Japanese Biochemical Society. All rights reserved.",
    "doi": "10.1093/jb/mvab047",
    "journal": "Journal of biochemistry",
    "keywords": [
        "JNK/NF-\u03baB signalling pathway",
        "apoptosis",
        "diabetic cardiomyopathy",
        "miR-20a-5p"
    ],
    "methods": null,
    "publication_date": "2021-04-11",
    "pubmed_id": "33837411",
    "results": null,
    "title": "MiR-20a-5p overexpression prevented diabetic cardiomyopathy via inhibition of cardiomyocyte apoptosis, hypertrophy, fibrosis and JNK/NF-\u03baB signalling pathway.",
    "xml": "<Element 'PubmedArticle' at 0x788504867880>"
}