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Creatine, guanidinoacetate and homoarginine in statin-induced myopathy

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Creatine, guanidinoacetate and homoarginine in statin-induced myopathy. / Neu, Axel; Hornig, Sönke; Sasani, Ali; Isbrandt, Dirk; Gerloff, Christian; Tsikas, Dimitris; Schwedhelm, Edzard; Choe, Chi-Un.

In: AMINO ACIDS, Vol. 52, No. 6-7, 07.2020, p. 1067-1069.

Research output: SCORING: Contribution to journal › Other (editorial matter etc.) › Research

Harvard

Neu, A, Hornig, S, Sasani, A, Isbrandt, D, Gerloff, C, Tsikas, D, Schwedhelm, E & Choe, C-U 2020, 'Creatine, guanidinoacetate and homoarginine in statin-induced myopathy', AMINO ACIDS, vol. 52, no. 6-7, pp. 1067-1069. https://doi.org/10.1007/s00726-020-02865-w

APA

Neu, A., Hornig, S., Sasani, A., Isbrandt, D., Gerloff, C., Tsikas, D., Schwedhelm, E., & Choe, C-U. (2020). Creatine, guanidinoacetate and homoarginine in statin-induced myopathy. AMINO ACIDS, 52(6-7), 1067-1069. https://doi.org/10.1007/s00726-020-02865-w

Vancouver

Neu A, Hornig S, Sasani A, Isbrandt D, Gerloff C, Tsikas D et al. Creatine, guanidinoacetate and homoarginine in statin-induced myopathy. AMINO ACIDS. 2020 Jul;52(6-7):1067-1069. https://doi.org/10.1007/s00726-020-02865-w

Bibtex

@article{47b48e636a314d3cab461950565f3e8b,
title = "Creatine, guanidinoacetate and homoarginine in statin-induced myopathy",
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.",
author = "Axel Neu and S{\"o}nke Hornig and Ali Sasani and Dirk Isbrandt and Christian Gerloff and Dimitris Tsikas and Edzard Schwedhelm and Chi-Un Choe",
note = "Letter",
year = "2020",
month = jul,
doi = "10.1007/s00726-020-02865-w",
language = "English",
volume = "52",
pages = "1067--1069",
journal = "AMINO ACIDS",
issn = "0939-4451",
publisher = "Springer Wien",
number = "6-7",

}

RIS

TY - JOUR

T1 - Creatine, guanidinoacetate and homoarginine in statin-induced myopathy

AU - Neu, Axel

AU - Hornig, Sönke

AU - Sasani, Ali

AU - Isbrandt, Dirk

AU - Gerloff, Christian

AU - Tsikas, Dimitris

AU - Schwedhelm, Edzard

AU - Choe, Chi-Un

N1 - Letter

PY - 2020/7

Y1 - 2020/7

N2 - 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.

AB - 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.

U2 - 10.1007/s00726-020-02865-w

DO - 10.1007/s00726-020-02865-w

M3 - Other (editorial matter etc.)

C2 - 32594255

VL - 52

SP - 1067

EP - 1069

JO - AMINO ACIDS

JF - AMINO ACIDS

SN - 0939-4451

IS - 6-7

ER -