Key result
Phosphocreatine administration ameliorated isoproterenol-induced cardiac fibrosis and cardiomyocyte apoptosis in rats by reducing collagen accumulation and blocking MAPK and NF-κB signaling pathways.
Why the study?
The study was designed to further explore the role and underlying molecular mechanism of phosphocreatine for cardiac fibrosis in vivo.
Does phosphocreatine prevent cardiac fibrosis and cardiomyocyte apoptosis in rats with isoproterenol-induced cardiac fibrosis?
Does phosphocreatine prevent cardiac fibrosis and cardiomyocyte apoptosis in rats with isoproterenol-induced cardiac fibrosis?
Phosphocreatine attenuates isoproterenol-induced cardiac fibrosis and cardiomyocyte apoptosis in a rat model by modulating MAPKs and NF-κB signaling pathways.
PCr may attenuate experimental cardiac fibrosis; leaves open any therapeutic role in human remodeling.
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.
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Dai et al. (2019) studied Isoproterenol-induced cardiac fibrosis. Phosphocreatine (PCr) vs. Isoproterenol (ISO) alone was evaluated on Cardiac fibrosis and cardiomyocyte apoptosis. Phosphocreatine administration ameliorated isoproterenol-induced cardiac fibrosis and cardiomyocyte apoptosis in rats by reducing collagen accumulation and blocking MAPK and NF-κB signaling pathways.
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