Alterations in peroxisome-mitochondria interplay in skeletal muscle accelerate muscle dysfunction

Marco Scalabrin, Eloisa Turco, Ilaria Davigo, Riccardo Filadi, Leonardo Nogara, Gaia Gherardi, Lucia Barazzuol, Andrea Armani, Giulia Trani, Samuele Negro, Anais Franco-Romero, Yorrick Jaspers, Elisa Baschiera, Rossella Cegli, Eugenio Prete, Tito Cali, Bert Blaauw, Leonardo Salviati, Michela Rigoni, Cristina Mammucari, Sylvie Caspar-Bauguil, Cedric Moro, Paola Pizzo, Marco Sandri, Stephan Kemp and Vanina Romanello ()
Additional contact information
Marco Scalabrin: University of Padova
Eloisa Turco: University of Padova
Ilaria Davigo: University of Padova
Riccardo Filadi: University of Padova
Leonardo Nogara: University of Padova
Gaia Gherardi: University of Padova
Lucia Barazzuol: University of Padova
Andrea Armani: University of Padova
Giulia Trani: University of Padova
Samuele Negro: University of Padova
Anais Franco-Romero: University of Padova
Yorrick Jaspers: Amsterdam University Medical Center, Amsterdam Gastroenterology Endocrinology Metabolism
Elisa Baschiera: University of Padova
Rossella Cegli: Telethon Institute of Genetics and Medicine (TIGEM)
Eugenio Prete: Telethon Institute of Genetics and Medicine (TIGEM)
Tito Cali: University of Padova
Bert Blaauw: University of Padova
Leonardo Salviati: University of Padova
Michela Rigoni: University of Padova
Cristina Mammucari: University of Padova
Sylvie Caspar-Bauguil: Toulouse University
Cedric Moro: Toulouse University
Paola Pizzo: University of Padova
Marco Sandri: University of Padova
Stephan Kemp: Amsterdam University Medical Center, Amsterdam Gastroenterology Endocrinology Metabolism
Vanina Romanello: University of Padova

Nature Communications, 2025, vol. 16, issue 1, 1-24

Abstract: Abstract Skeletal muscles, which constitute 40–50% of body mass, regulate whole-body energy expenditure and glucose and lipid metabolism. Peroxisomes are dynamic organelles that play a crucial role in lipid metabolism and clearance of reactive oxygen species, however their role in skeletal muscle remains poorly understood. To clarify this issue, we generated a muscle-specific transgenic mouse line with peroxisome import deficiency through the deletion of peroxisomal biogenesis factor 5 (Pex5). Here, we show that Pex5 inhibition results in impaired lipid metabolism, reduced muscle force and exercise performance. Moreover, mitochondrial structure, content, and function are also altered, accelerating the onset of age-related structural defects, neuromuscular junction degeneration, and muscle atrophy. Consistent with these observations, we observe a decline in peroxisomal content in the muscles of control mice undergoing natural aging. Altogether, our findings show the importance of preserving peroxisomal function and their interplay with mitochondria to maintain muscle health during aging.

Date: 2025
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DOI: 10.1038/s41467-025-64833-w

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