New evidence of exercise training benefits in myostatin-deficient mice: Effect on lipidomic abnormalities

Baati, Narjès; Feillet‐Coudray, Christine; Fouret, Gilles; Vernus, Barbara; Goustard, Bénédicte; Jollet, Maxence; Bertrand‐Gaday, Christelle; Coudray, Charles; Lecomte, Jérôme; Bonnieu, Anne; Koechlin-Ramonatxo, Christelle

doi:10.1016/j.bbrc.2019.06.014

Cited by 12 publications

(5 citation statements)

References 30 publications

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“…This suggests that MSTN may affect mitochondrial function by regulating lipid composition in mitochondrial membrane. Interestingly, the abnormal cardiolipin content in muscle mitochondrial membrane caused by MSTN deficiency can be corrected by endurance training ( 40 ).…”

Section: Mstn In Regulating Cell Metabolismmentioning

confidence: 99%

Myostatin: a potential therapeutic target for metabolic syndrome

et al. 2023

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Metabolic syndrome is a complex metabolic disorder, its main clinical manifestations are obesity, hyperglycemia, hypertension and hyperlipidemia. Although metabolic syndrome has been the focus of research in recent decades, it has been proposed that the occurrence and development of metabolic syndrome is related to pathophysiological processes such as insulin resistance, adipose tissue dysfunction and chronic inflammation, but there is still a lack of favorable clinical prevention and treatment measures for metabolic syndrome. Multiple studies have shown that myostatin (MSTN), a member of the TGF-β family, is involved in the development and development of obesity, hyperlipidemia, diabetes, and hypertension (clinical manifestations of metabolic syndrome), and thus may be a potential therapeutic target for metabolic syndrome. In this review, we describe the transcriptional regulation and receptor binding pathway of MSTN, then introduce the role of MSTN in regulating mitochondrial function and autophagy, review the research progress of MSTN in metabolic syndrome. Finally summarize some MSTN inhibitors under clinical trial and proposed the use of MSTN inhibitor as a potential target for the treatment of metabolic syndrome.

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Section: Mstn In Regulating Cell Metabolismmentioning

confidence: 99%

Myostatin: a potential therapeutic target for metabolic syndrome

et al. 2023

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“…Myostatin (MSTN) is one of the main genetic determinants of the type of muscle fibers, it is related to strength and endurance [ 51 ]: it inhibits the proliferation and differentiation of myoblasts in muscle development [ 52 ], which limits muscle growth and is produced mainly in skeletal muscles [ 53 ]. Therefore, inactivation or inhibition of myostatin promotes muscle growth [ 54 ]. However, studies in mice have found that mice deficient in MSTN have fewer mitochondria, consequently leading to changes in skeletal muscle activity and enzyme capacity.…”

Section: Markers Potentially Associated With Mitochondrial Dysfunctio...mentioning

confidence: 99%

Mitochondrial Dysfunctions and Potential Molecular Markers in Sport Horses

Dzięgielewska

Dunisławska

2022

IJMS

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Mitochondria are an essential part of most eukaryotic cells. The crucial role of these organelles is the production of metabolic energy, which is converted into ATP in oxidative phosphorylation. They are also involved in and constitute apoptosis, the site of many metabolic processes. Some of the factors that negatively affect mitochondria are stress, excessive exercise, disease, and the aging process. Exercise can cause the release of large amounts of free radicals, inflammation, injury, and stress. All of these factors can contribute to mitochondrial dysfunction, which can consistently lead to inflammatory responses, tissue damage, organ dysfunction, and a host of diseases. The functions of the mitochondria and the consequences of their disturbance can be of great importance in the breeding and use of horses. The paper reviews mitochondrial disorders in horses and, based on the literature, indicates genetic markers strongly related to this issue.

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“…As a side note, one concern of blocking ACVR2 signaling in muscle was associated with negative changes in muscle oxidative metabolism in healthy and dystrophic mice [165,176]. Therefore, exercise as a co-treatment to prevent such changes has been suggested based on promising results in preclinical trials [176,177]. However, this effect of blocking ACVR2 signaling seems to be context-dependent, as in tumor-bearing mice, counteraction of myostatin [158] or ACVR2 ligands [35] was not shown to affect the muscle oxidative metabolism.…”

Section: Effects Of Blocking Acvr2 Signaling On Skeletal Musclementioning

confidence: 99%

Targeting the Activin Receptor Signaling to Counteract the Multi-Systemic Complications of Cancer and Its Treatments

Hulmi

Nissinen

Penna

et al. 2021

Cells

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Muscle wasting, i.e., cachexia, frequently occurs in cancer and associates with poor prognosis and increased morbidity and mortality. Anticancer treatments have also been shown to contribute to sustainment or exacerbation of cachexia, thus affecting quality of life and overall survival in cancer patients. Pre-clinical studies have shown that blocking activin receptor type 2 (ACVR2) or its ligands and their downstream signaling can preserve muscle mass in rodents bearing experimental cancers, as well as in chemotherapy-treated animals. In tumor-bearing mice, the prevention of skeletal and respiratory muscle wasting was also associated with improved survival. However, the definitive proof that improved survival directly results from muscle preservation following blockade of ACVR2 signaling is still lacking, especially considering that concurrent beneficial effects in organs other than skeletal muscle have also been described in the presence of cancer or following chemotherapy treatments paired with counteraction of ACVR2 signaling. Hence, here, we aim to provide an up-to-date literature review on the multifaceted anti-cachectic effects of ACVR2 blockade in preclinical models of cancer, as well as in combination with anticancer treatments.

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New evidence of exercise training benefits in myostatin-deficient mice: Effect on lipidomic abnormalities

Cited by 12 publications

References 30 publications

Myostatin: a potential therapeutic target for metabolic syndrome

Myostatin: a potential therapeutic target for metabolic syndrome

Mitochondrial Dysfunctions and Potential Molecular Markers in Sport Horses

Targeting the Activin Receptor Signaling to Counteract the Multi-Systemic Complications of Cancer and Its Treatments

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