| Home > Publications Database > Creatine, guanidinoacetate and homoarginine in statin-induced myopathy. > print |
| 001 | 153374 | ||
| 005 | 20240321221043.0 | ||
| 024 | 7 | _ | |a 10.1007/s00726-020-02865-w |2 doi |
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| 024 | 7 | _ | |a 0939-4451 |2 ISSN |
| 024 | 7 | _ | |a 1438-2199 |2 ISSN |
| 037 | _ | _ | |a DZNE-2020-01371 |
| 041 | _ | _ | |a English |
| 082 | _ | _ | |a 540 |
| 100 | 1 | _ | |a Neu, Axel |b 0 |
| 245 | _ | _ | |a Creatine, guanidinoacetate and homoarginine in statin-induced myopathy. |
| 260 | _ | _ | |a Wien [u.a.] |c 2020 |b Springer |
| 336 | 7 | _ | |a article |2 DRIVER |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1606141744_31133 |2 PUB:(DE-HGF) |x Letter |
| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
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| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 520 | _ | _ | |a 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. |
| 536 | _ | _ | |a 342 - Disease Mechanisms and Model Systems (POF3-342) |0 G:(DE-HGF)POF3-342 |c POF3-342 |f POF III |x 0 |
| 588 | _ | _ | |a Dataset connected to CrossRef, PubMed, |
| 650 | _ | 2 | |a Amidinotransferases: deficiency |2 MeSH |
| 650 | _ | 2 | |a Amino Acid Metabolism, Inborn Errors |2 MeSH |
| 650 | _ | 2 | |a Animals |2 MeSH |
| 650 | _ | 2 | |a Creatine: metabolism |2 MeSH |
| 650 | _ | 2 | |a Creatine: pharmacology |2 MeSH |
| 650 | _ | 2 | |a Developmental Disabilities |2 MeSH |
| 650 | _ | 2 | |a Glycine: analogs & derivatives |2 MeSH |
| 650 | _ | 2 | |a Glycine: metabolism |2 MeSH |
| 650 | _ | 2 | |a Guanidinoacetate N-Methyltransferase: deficiency |2 MeSH |
| 650 | _ | 2 | |a Homoarginine: metabolism |2 MeSH |
| 650 | _ | 2 | |a Hydroxymethylglutaryl-CoA Reductase Inhibitors |2 MeSH |
| 650 | _ | 2 | |a Intellectual Disability |2 MeSH |
| 650 | _ | 2 | |a Mice |2 MeSH |
| 650 | _ | 2 | |a Muscular Diseases: chemically induced |2 MeSH |
| 650 | _ | 2 | |a Muscular Diseases: metabolism |2 MeSH |
| 650 | _ | 2 | |a Phosphocreatine: metabolism |2 MeSH |
| 650 | _ | 2 | |a Speech Disorders |2 MeSH |
| 700 | 1 | _ | |a Hornig, Sönke |b 1 |
| 700 | 1 | _ | |a Sasani, Ali |b 2 |
| 700 | 1 | _ | |a Isbrandt, Dirk |0 P:(DE-2719)2810976 |b 3 |u dzne |
| 700 | 1 | _ | |a Gerloff, Christian |b 4 |
| 700 | 1 | _ | |a Tsikas, Dimitris |b 5 |
| 700 | 1 | _ | |a Schwedhelm, Edzard |b 6 |
| 700 | 1 | _ | |a Choe, Chi-Un |0 P:(DE-HGF)0 |b 7 |e Corresponding author |
| 773 | _ | _ | |a 10.1007/s00726-020-02865-w |g Vol. 52, no. 6-7, p. 1067 - 1069 |0 PERI:(DE-600)1480643-5 |n 6-7 |p 1067 - 1069 |t Amino acids |v 52 |y 2020 |x 1438-2199 |
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