Growth and differentiation factor 15 as a biomarker for mitochondrial myopathy. Poulsen, N. S., Madsen, K. L., Hornsyld, T. M., Eisum, A. V., Fornander, F., Buch, A. E., Stemmerik, M. G., Ruiz-Ruiz, C., Krag, T. O., & Vissing, J. Mitochondrion, 50:35–41, January, 2020. Edition: 20191026![Growth and differentiation factor 15 as a biomarker for mitochondrial myopathy [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex OBJECTIVE: We investigated if Growth and Differentiation Factor 15 (GDF-15) can be used as a biomarker to distinguish patients with mitochondrial myopathy from patients with other myopathies. METHODS: Serum GDF-15 was measured in 28 patients with mitochondrial disease, 24 with metabolic myopathies, 27 with muscular dystrophy and 21 healthy controls. RESULTS AND CONCLUSIONS: Our findings indicate that elevated GDF-15 can distinguish patients with mitochondrial myopathy from other myopathies, including metabolic myopathies. This suggests that increases in GDF-15 is specific to respiratory chain dysfunction rather than general metabolic dysfunction or muscle defect.
@article{poulsen2020,
title = {Growth and differentiation factor 15 as a biomarker for mitochondrial myopathy},
volume = {50},
issn = {1872-8278 (Electronic) 1567-7249 (Linking)},
url = {https://www.ncbi.nlm.nih.gov/pubmed/31669236},
doi = {10.1016/j.mito.2019.10.005},
abstract = {OBJECTIVE: We investigated if Growth and Differentiation Factor 15 (GDF-15) can be used as a biomarker to distinguish patients with mitochondrial myopathy from patients with other myopathies. METHODS: Serum GDF-15 was measured in 28 patients with mitochondrial disease, 24 with metabolic myopathies, 27 with muscular dystrophy and 21 healthy controls. RESULTS AND CONCLUSIONS: Our findings indicate that elevated GDF-15 can distinguish patients with mitochondrial myopathy from other myopathies, including metabolic myopathies. This suggests that increases in GDF-15 is specific to respiratory chain dysfunction rather than general metabolic dysfunction or muscle defect.},
journal = {Mitochondrion},
author = {Poulsen, N. S. and Madsen, K. L. and Hornsyld, T. M. and Eisum, A. V. and Fornander, F. and Buch, A. E. and Stemmerik, M. G. and Ruiz-Ruiz, C. and Krag, T. O. and Vissing, J.},
month = jan,
year = {2020},
note = {Edition: 20191026},
keywords = {Humans, Adult, Male, Female, Middle Aged, Adolescent, Aged, Young Adult, Oxidative Stress, Biomarkers/blood/metabolism, Exercise, Exercise Test, Gene Expression Regulation/physiology, Growth and differentiation factor 15, Growth Differentiation Factor 15/*blood, Metabolic myopathy, Mitochondrial Myopathies/genetics/*metabolism, Mitochondrial myopathy, Muscular dystrophy, Pilot Projects},
pages = {35--41},
annote = {Poulsen, Nanna ScharffMadsen, Karen LindhardtHornsyld, Tessa MunkeboeEisum, Anne-Sofie VibaekFornander, FrejaBuch, Astrid EmilieStemmerik, Mads GodtfeldtRuiz-Ruiz, CristinaKrag, Thomas OliverVissing, JohnengResearch Support, Non-U.S. Gov'tNetherlands2019/11/02Mitochondrion. 2020 Jan;50:35-41. doi: 10.1016/j.mito.2019.10.005. Epub 2019 Oct 26.},
}
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METHODS: Serum GDF-15 was measured in 28 patients with mitochondrial disease, 24 with metabolic myopathies, 27 with muscular dystrophy and 21 healthy controls. RESULTS AND CONCLUSIONS: Our findings indicate that elevated GDF-15 can distinguish patients with mitochondrial myopathy from other myopathies, including metabolic myopathies. This suggests that increases in GDF-15 is specific to respiratory chain dysfunction rather than general metabolic dysfunction or muscle defect.","journal":"Mitochondrion","author":[{"propositions":[],"lastnames":["Poulsen"],"firstnames":["N.","S."],"suffixes":[]},{"propositions":[],"lastnames":["Madsen"],"firstnames":["K.","L."],"suffixes":[]},{"propositions":[],"lastnames":["Hornsyld"],"firstnames":["T.","M."],"suffixes":[]},{"propositions":[],"lastnames":["Eisum"],"firstnames":["A.","V."],"suffixes":[]},{"propositions":[],"lastnames":["Fornander"],"firstnames":["F."],"suffixes":[]},{"propositions":[],"lastnames":["Buch"],"firstnames":["A.","E."],"suffixes":[]},{"propositions":[],"lastnames":["Stemmerik"],"firstnames":["M.","G."],"suffixes":[]},{"propositions":[],"lastnames":["Ruiz-Ruiz"],"firstnames":["C."],"suffixes":[]},{"propositions":[],"lastnames":["Krag"],"firstnames":["T.","O."],"suffixes":[]},{"propositions":[],"lastnames":["Vissing"],"firstnames":["J."],"suffixes":[]}],"month":"January","year":"2020","note":"Edition: 20191026","keywords":"Humans, Adult, Male, Female, Middle Aged, Adolescent, Aged, Young Adult, Oxidative Stress, Biomarkers/blood/metabolism, Exercise, Exercise Test, Gene Expression Regulation/physiology, Growth and differentiation factor 15, Growth Differentiation Factor 15/*blood, Metabolic myopathy, Mitochondrial Myopathies/genetics/*metabolism, Mitochondrial myopathy, Muscular dystrophy, Pilot Projects","pages":"35–41","annote":"Poulsen, Nanna ScharffMadsen, Karen LindhardtHornsyld, Tessa MunkeboeEisum, Anne-Sofie VibaekFornander, FrejaBuch, Astrid EmilieStemmerik, Mads GodtfeldtRuiz-Ruiz, CristinaKrag, Thomas OliverVissing, JohnengResearch Support, Non-U.S. Gov'tNetherlands2019/11/02Mitochondrion. 2020 Jan;50:35-41. doi: 10.1016/j.mito.2019.10.005. 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This suggests that increases in GDF-15 is specific to respiratory chain dysfunction rather than general metabolic dysfunction or muscle defect.},\n\tjournal = {Mitochondrion},\n\tauthor = {Poulsen, N. S. and Madsen, K. L. and Hornsyld, T. M. and Eisum, A. V. and Fornander, F. and Buch, A. E. and Stemmerik, M. G. and Ruiz-Ruiz, C. and Krag, T. 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