Fluvastatin-induced myofibrillar damage is associated with elevated ROS, and impaired fatty acid oxidation, and is preceded by mitochondrial morphological changes.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
09 Feb 2024
Historique:
received: 05 12 2023
accepted: 31 01 2024
medline: 10 2 2024
pubmed: 10 2 2024
entrez: 9 2 2024
Statut: epublish

Résumé

Previously, we showed that fluvastatin treatment induces myofibrillar damage and mitochondrial phenotypes in the skeletal muscles of Drosophila. However, the sequential occurrence of mitochondrial phenotypes and myofibril damage remains elusive. To address this, we treated flies with fluvastatin for two and five days and examined their thorax flight muscles using confocal microscopy. In the two-day fluvastatin group, compared to the control, thorax flight muscles exhibited mitochondrial morphological changes, including fragmentation, rounding up and reduced content, while myofibrils remained organized in parallel. In the five-day fluvastatin treatment, not only did mitochondrial morphological changes become more pronounced, but myofibrils became severely disorganized with significantly increased thickness and spacing, along with myofilament abnormalities, suggesting myofibril damage. These findings suggest that fluvastatin-induced mitochondrial changes precede myofibril damage. Moreover, in the five-day fluvastatin group, the mitochondria demonstrated elevated H

Identifiants

pubmed: 38336990
doi: 10.1038/s41598-024-53446-w
pii: 10.1038/s41598-024-53446-w
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

3338

Subventions

Organisme : Vetenskapsrådet
ID : 2019-01066
Organisme : Vetenskapsrådet
ID : 2019-01066
Organisme : Vetenskapsrådet
ID : 2019-01066
Organisme : AFM-Telethon trampoline grant
ID : 23108
Organisme : AFM-Telethon trampoline grant
ID : 23108

Informations de copyright

© 2024. The Author(s).

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Auteurs

Mohamed H Al-Sabri (MH)

Department of Surgical Sciences, Division of Functional Pharmacology and Neuroscience, Biomedical Center (BMC), Uppsala University, Husargatan 3, 751 24, Uppsala, Sweden. mohamed.alsabri@uu.se.
Department of Pharmaceutical Biosciences, Uppsala University, 751 24, Uppsala, Sweden. mohamed.alsabri@uu.se.

Nourhane Ammar (N)

Institut de Génétique Et Développement de Rennes (IGDR), Université de Rennes, CNRS, UMR6290, 35065, Rennes, France.

Stanislava Korzh (S)

Latvian Institute of Organic Synthesis, Aizkraukles 21, Riga, 1006, Latvia.

Ahmed M Alsehli (AM)

Department of Surgical Sciences, Division of Functional Pharmacology and Neuroscience, Biomedical Center (BMC), Uppsala University, Husargatan 3, 751 24, Uppsala, Sweden.
Faculty of Medicine, King Abdulaziz University and Hospital, Al Ehtifalat St., 21589, Jeddah, Saudi Arabia.

Kimia Hosseini (K)

Department of Pharmaceutical Biosciences, Uppsala University, 751 24, Uppsala, Sweden.

Robert Fredriksson (R)

Department of Pharmaceutical Biosciences, Uppsala University, 751 24, Uppsala, Sweden.

Jessica Mwinyi (J)

Department of Surgical Sciences, Division of Functional Pharmacology and Neuroscience, Biomedical Center (BMC), Uppsala University, Husargatan 3, 751 24, Uppsala, Sweden.

Michael J Williams (MJ)

Department of Surgical Sciences, Division of Functional Pharmacology and Neuroscience, Biomedical Center (BMC), Uppsala University, Husargatan 3, 751 24, Uppsala, Sweden.

Hadi Boukhatmi (H)

Institut de Génétique Et Développement de Rennes (IGDR), Université de Rennes, CNRS, UMR6290, 35065, Rennes, France.

Helgi B Schiöth (HB)

Department of Surgical Sciences, Division of Functional Pharmacology and Neuroscience, Biomedical Center (BMC), Uppsala University, Husargatan 3, 751 24, Uppsala, Sweden. helgi.schioth@neuro.uu.se.

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