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@ARTICLE{Neu:153374,
      author       = {Neu, Axel and Hornig, Sönke and Sasani, Ali and Isbrandt,
                      Dirk and Gerloff, Christian and Tsikas, Dimitris and
                      Schwedhelm, Edzard and Choe, Chi-Un},
      title        = {{C}reatine, guanidinoacetate and homoarginine in
                      statin-induced myopathy.},
      journal      = {Amino acids},
      volume       = {52},
      number       = {6-7},
      issn         = {1438-2199},
      address      = {Wien [u.a.]},
      publisher    = {Springer},
      reportid     = {DZNE-2020-01371},
      pages        = {1067 - 1069},
      year         = {2020},
      abstract     = {Our study evaluated the effect of creatine and homoarginine
                      in AGAT- and GAMT-deficient mice after simvastatin exposure.
                      Balestrino and Adriano suggest that guanidinoacetate might
                      explain the difference between AGAT- and GAMT-deficient mice
                      in simvastatin-induced myopathy. We agree with Balestrino
                      and Adriano that our data shows that (1) creatine possesses
                      a protective potential to ameliorate statin-induced myopathy
                      in humans and mice and (2) homoarginine did not reveal a
                      beneficial effect in statin-induced myopathy. Third, we
                      agree that guanidinoacetate can be phosphorylated and
                      partially compensate for phosphocreatine. In our study,
                      simvastatin-induced damage showed a trend to be less
                      pronounced in GAMT-deficient mice compared with wildtype
                      mice. Therefore, (phospo) guanidinoacetate cannot completely
                      explain the milder phenotype of GAMT-deficient mice, but we
                      agree that it might contribute to ameliorate statin-induced
                      myopathy in GAMT-deficient mice compared with AGAT-deficient
                      mice. Finally, we agree with Balestino and Adriano that AGAT
                      metabolites should further be evaluated as potential
                      treatments in statin-induced myopathy.},
      subtyp        = {Letter},
      keywords     = {Amidinotransferases: deficiency / Amino Acid Metabolism,
                      Inborn Errors / Animals / Creatine: metabolism / Creatine:
                      pharmacology / Developmental Disabilities / Glycine: analogs
                      $\&$ derivatives / Glycine: metabolism / Guanidinoacetate
                      N-Methyltransferase: deficiency / Homoarginine: metabolism /
                      Hydroxymethylglutaryl-CoA Reductase Inhibitors /
                      Intellectual Disability / Mice / Muscular Diseases:
                      chemically induced / Muscular Diseases: metabolism /
                      Phosphocreatine: metabolism / Speech Disorders},
      cin          = {AG Isbrandt},
      ddc          = {540},
      cid          = {I:(DE-2719)1011003},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32594255},
      pmc          = {pmc:PMC7406479},
      doi          = {10.1007/s00726-020-02865-w},
      url          = {https://pub.dzne.de/record/153374},
}