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Flvcr1a deficiency promotes heme-based energy metabolism dysfunction in skeletal muscle

Academic Article
Publication Date:
2024
Citation:
Flvcr1a deficiency promotes heme-based energy metabolism dysfunction in skeletal muscle / M. Mistretta, V. Fiorito, A.L. Allocco, G. Ammirata, M.Y. Hsu, S. Digiovanni, M. Belicchi, L. Napoli, M. Ripolone, E. Trombetta, P. Mauri, A. Farini, M. Meregalli, C. Villa, P.E. Porporato, B. Miniscalco, S.G. Crich, C. Riganti, Y. Torrente, E. Tolosano. - In: CELL REPORTS. - ISSN 2211-1247. - 43:3(2024 Mar 26), pp. 113854.1-113854.21. [10.1016/j.celrep.2024.113854]
abstract:
The definition of cell metabolic profile is essential to ensure skeletal muscle fiber heterogeneity and to achieve a proper equilibrium between the self-renewal and commitment of satellite stem cells. Heme sustains several biological functions, including processes profoundly implicated with cell metabolism. The skeletal muscle is a significant heme-producing body compartment, but the consequences of impaired heme homeostasis on this tissue have been poorly investigated. Here, we generate a skeletal-muscle-specific feline leukemia virus subgroup C receptor 1a (FLVCR1a) knockout mouse model and show that, by sustaining heme synthesis, FLVCR1a contributes to determine the energy phenotype in skeletal muscle cells and to modulate satellite cell differentiation and muscle regeneration.
IRIS type:
01 - Articolo su periodico
Keywords:
ALAS1; CP: Metabolism; FLVCR1; FLVCR1a; heme; metabolism; skeletal muscle;
List of contributors:
M. Mistretta, V. Fiorito, A.L. Allocco, G. Ammirata, M.Y. Hsu, S. Digiovanni, M. Belicchi, L. Napoli, M. Ripolone, E. Trombetta, P. Mauri, A. Farini, M. Meregalli, C. Villa, P.E. Porporato, B. Miniscalco, S.G. Crich, C. Riganti, Y. Torrente, E. Tolosano
Authors of the University:
TORRENTE YVAN ( author )
VILLA CHIARA ( author )
Link to information sheet:
https://air.unimi.it/handle/2434/1079608
Full Text:
https://air.unimi.it/retrieve/handle/2434/1079608/2484352/1-s2.0-S2211124724001827-main.pdf
Project:
Disentangling genetic, epigenetic and hormonal regulation of Fe/heme metabolism in the gender-specific nature of NAFLD (DEFENDER)
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