Phosphocreatine Attenuates Isoproterenol-Induced Cardiac Fibrosis and Cardiomyocyte Apoptosis.

The present study was designed to further explore the role and the underlying molecular mechanism of phosphocreatine (PCr) for cardiac fibrosis in vivo. Isoproterenol (ISO) was used to induce cardiac fibrosis in rats. PCr administration ameliorated fibrosis by reducing collagen accumulation and fibr...

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Publicado en:BioMed Research International pp. 1 - 8
Autores principales: Dai, Hui, Chen, Liang, Gao, Dongyue, Fei, Aihua
Formato: pictorial research tables/charts Journal Article
Publicado: Wiley-Blackwell 1/8/2019
Acceso en línea:Ver este registro en EBSCOhost
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      dt: 1/8/2019
      pid: 480
      pub: Wiley-Blackwell
      place: Malden, Massachusetts
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        134223810
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        10.1155/2019/5408289
        134223810
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        atl: Phosphocreatine Attenuates Isoproterenol-Induced Cardiac Fibrosis and Cardiomyocyte Apoptosis.
      aug:
        au:
          Dai, Hui
          Chen, Liang
          Gao, Dongyue
          Fei, Aihua
        affil: Department of Emergency, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China
      sug:
        subj:
          Fibrosis Prevention and Control
          Phosphocreatine Pharmacodynamics
          Myocytes, Cardiac Drug Effects
          Apoptosis Drug Effects
          Isoproterenol
          Animal Studies
          Rats
          In Vivo Studies
          Transforming Growth Factor beta Drug Effects
          Muscle Proteins Drug Effects
          Collagen Drug Effects
          Protein Kinases Drug Effects
          NF-kappa B Drug Effects
          Signal Transduction Drug Effects
          Matrix Metalloproteinases Drug Effects
          Caspases Drug Effects
          Gene Expression Drug Effects
      ab: The present study was designed to further explore the role and the underlying molecular mechanism of phosphocreatine (PCr) for cardiac fibrosis in vivo. Isoproterenol (ISO) was used to induce cardiac fibrosis in rats. PCr administration ameliorated fibrosis by reducing collagen accumulation and fibrosis-related signals, including transforming growth factor beta 1 (TGF-β1), alpha smooth muscle actin (α-SMA), collagen type I, and collagen type III. Mitogen-activated protein kinases (MAPKs) and nuclear factor kappa B (NF-κB) signaling pathways, including p38, extracellular signal regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p65, were highly activated by ISO and blocked by PCr. Moreover, PCr decreased ISO-induced matrix metalloproteinase-9 (MMP-9) and increased the tissue inhibitor of metalloproteinase-1 (TIMP-1) expression. Furthermore, PCr suppressed cardiomyocyte apoptosis induced by ISO, as shown by downregulated expression of the proapoptotic caspase-3, Bax, and upregulated expression of the antiapoptotic Bcl-2. Taken together, PCr can be an effective agent for preventing cardiac fibrosis and cardiomyocyte apoptosis.
      pubtype: Academic Journal
      doctype:
        pictorial
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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