Sarcopenia: nothing is as it seems. Author's response to Gonzalez, Cruz-Jentoft, Phillips and Prado DOI
Federico Bozzetti

Current Opinion in Clinical Nutrition & Metabolic Care, Год журнала: 2024, Номер 27(6), С. 527 - 528

Опубликована: Окт. 3, 2024

Язык: Английский

Mitophagy is required to protect against excessive skeletal muscle atrophy following hindlimb immobilization DOI Creative Commons
Fasih A. Rahman, Michelle M. Graham,

Albert Adam

и другие.

Journal of Biomedical Science, Год журнала: 2025, Номер 32(1)

Опубликована: Фев. 18, 2025

Skeletal muscle atrophy involves significant remodeling of fibers and is characterized by deficits in mitochondrial content function. These changes are intimately connected to shifts turnover, encompassing processes such as mitophagy biogenesis. However, the role these turnover remains poorly understood. We used a novel reporter model, mt-Keima mice, perform hindlimb immobilization accurately measure mitophagy. A comprehensive set analyses were conducted investigate biochemical molecular at levels. also performed image determine mitophagic flux. To further explore immobilization-induced atrophy, we treated animals with N-acetylcysteine (NAC; 150 mg/kg/day) modify reactive oxygen species (ROS) signaling colchicine (0.4 inhibit autophagy. Our study revealed that leads weakness fast-twitch (types IIA, IIX, IIB), recovery observed IIA following remobilization. This was accompanied increase Additionally, induced notable dysfunction, shown diminished respiration, increased ROS, greater whole lipid peroxidation. Treatment immobilized mice NAC enhanced respiration reduced ROS generation but suppressed flux intensified type IIX IIB fibers. administration flux, which exacerbated Colchicine treatment led reductions function, CASP9 CASP3 activation. findings emphasize limiting excessive during immobilization. Targeting may offer new strategies preserve function prolonged periods

Язык: Английский

Процитировано

0

Aconiti Lateralis Radix Praeparata ameliorates heart failure via PI3K/AKT/Bnip3 pathway DOI Creative Commons
Wenxiu Liu,

Xingju Zou,

Yang Zheng

и другие.

Frontiers in Pharmacology, Год журнала: 2025, Номер 16

Опубликована: Март 26, 2025

Background Chronic heart failure (CHF) is one of the leading causes high mortality worldwide. It characterized by pathological hypertrophy and poses a major threat to human health. Aconiti Lateralis Radix Praeparata widely used in ancient China treat CHF. However, pathology obscured, necessitating further exploration. Methods Prospective targets were predicted network analysis. A transverse aortic constriction (TAC) mice model was subsequently constructed determine effects aqueous extract (AEA) on The echocardiography performed investigate cardiac function. Histopathological analysis tissue conducted assess myocardial fibrosis. Nontargeted metabolomics analyze serum metabolites. phosphorylation level PI3K AKT, downstream such as Bnip3, p62, Atg5, LC3II measured Western blotting. In vitro , norepinephrine (NE) stimulate hypertrophy. Parameters reactive oxygen species levels, mitochondrial membrane potential, ATP concentration, CK/MB content detected H9c2 cells. Results AEA significantly alleviated Network indicated participation AKT CHF, modulated Praeparata. vivo administration effectively ameliorated performance, evidenced elevation ejection fraction. displayed diminishment collagen fiber. Metabolomics showed that several metabolites tetrahydroxycorticosterone, decylubiquinone taurocholic acid increased TAC serum. Additionally, levels expression Drp1, Opa1, Atg5 altered group. NE stimulation cell surface area deteriorated functions partially reversed results, mechanism associated with mitophagy. Conclusion This study revealed improved function via PI3K/AKT/Bnip3 pathway.

Язык: Английский

Процитировано

0

Extracellular matrix in skeletal muscle injury and atrophy: mechanisms and therapeutic implications DOI Creative Commons
Xiaoyang Ge,

Yesheng Jin,

Jingyuan He

и другие.

Journal of Orthopaedic Translation, Год журнала: 2025, Номер 52, С. 404 - 418

Опубликована: Май 1, 2025

Язык: Английский

Процитировано

0

Polysaccharides targeting autophagy to alleviate metabolic syndrome DOI
Hongxia Li, Zeting Ye, Guangjuan Zheng

и другие.

International Journal of Biological Macromolecules, Год журнала: 2024, Номер 283, С. 137393 - 137393

Опубликована: Ноя. 7, 2024

Язык: Английский

Процитировано

1

Muscle loss: does one size fit all? A comment on Bozzetti's paper DOI
Marı́a Cristina González, Alfonso J. Cruz‐Jentoft, Stuart M. Phillips

и другие.

Current Opinion in Clinical Nutrition & Metabolic Care, Год журнала: 2024, Номер 27(6), С. 523 - 526

Опубликована: Авг. 26, 2024

Процитировано

0

Sarcopenia: nothing is as it seems. Author's response to Gonzalez, Cruz-Jentoft, Phillips and Prado DOI
Federico Bozzetti

Current Opinion in Clinical Nutrition & Metabolic Care, Год журнала: 2024, Номер 27(6), С. 527 - 528

Опубликована: Окт. 3, 2024

Язык: Английский

Процитировано

0