Multiple organ dysfunction - we must take a closer look at muscle wasting!

Teixeira, Cassiano; Neto, Felippe Leopoldo Dexheimer; Rosa, Régis Goulart

doi:10.5935/0103-507x.20190021

Cited by 2 publications

(3 citation statements)

References 5 publications

(12 reference statements)

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“…The number of CKD patients accounted for 9.1% of the world’s total population in 2017, which resulted in 1.2 million deaths each year ( GBD Chronic Kidney Disease Collaboration, 2020 ) and greatly increased the economic burden. In CKD patients, persistent imbalances between protein degradation and synthesis result in skeletal muscle atrophy, which is closely related to the rate of morbidity and mortality in CKD patients ( Zhang et al, 2018 ; Teixeira et al, 2019 ; Watanabe et al, 2019 ). The prevalence of muscular protein mass in CKD ranges from 4% to 63% depending on the different operational criteria ( Lamarca et al, 2014 ; D'Alessandro et al, 2018 ; Hanatani et al, 2018 ; Slee et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

Paeoniflorin Ameliorates Skeletal Muscle Atrophy in Chronic Kidney Disease via AMPK/SIRT1/PGC-1α-Mediated Oxidative Stress and Mitochondrial Dysfunction

Huang

et al. 2022

Front. Pharmacol.

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Skeletal muscle atrophy is a common and serious complication of chronic kidney disease (CKD). Oxidative stress and mitochondrial dysfunction are involved in the pathogenesis of muscle atrophy. The aim of this study was to explore the effects and mechanisms of paeoniflorin on CKD skeletal muscle atrophy. We demonstrated that paeoniflorin significantly improved renal function, calcium/phosphorus disorders, nutrition index and skeletal muscle atrophy in the 5/6 nephrectomized model rats. Paeoniflorin ameliorated the expression of proteins associated with muscle atrophy and muscle differentiation, including muscle atrophy F-box (MAFbx/atrogin-1), muscle RING finger 1 (MuRF1), MyoD and myogenin (MyoG). In addition, paeoniflorin modulated redox homeostasis by increasing antioxidant activity and suppressing excessive accumulation of reactive oxygen species (ROS). Paeoniflorin alleviated mitochondrial dysfunction by increasing the activities of electron transport chain complexes and mitochondrial membrane potential. Furthermore, paeoniflorin also regulates mitochondrial dynamics. Importantly, paeoniflorin upregulated the expression of silent information regulator 1 (SIRT1), peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α), and phosphorylation of AMP-activated protein kinase (AMPK). Similar results were observed in C2C12 myoblasts treated with TNF-α and paeoniflorin. Notably, these beneficial effects of paeoniflorin on muscle atrophy were abolished by inhibiting AMPK and SIRT1 and knocking down PGC-1α. Taken together, this study showed for the first time that paeoniflorin has great therapeutic potential for CKD skeletal muscle atrophy through AMPK/SIRT1/PGC-1α-mediated oxidative stress and mitochondrial dysfunction.

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Section: Introductionmentioning

confidence: 99%

Paeoniflorin Ameliorates Skeletal Muscle Atrophy in Chronic Kidney Disease via AMPK/SIRT1/PGC-1α-Mediated Oxidative Stress and Mitochondrial Dysfunction

Huang

et al. 2022

Front. Pharmacol.

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“…Muscle atrophy is the main pathophysiological consequence and the most effective marker of protein‐energy wasting, which is a well‐established complication in individuals with chronic kidney disease (CKD) 1 . Muscle atrophy is closely related to aggravated occurrence of other complications, such as infection and multiple organ failure 2 . It affects patients' quality of life and can result in increased morbidity and mortality.…”

Section: Introductionmentioning

confidence: 99%

“…1 Muscle atrophy is closely related to aggravated occurrence of other complications, such as infection and multiple organ failure. 2 It affects patients' quality of life and can result in increased morbidity and mortality. In recent decades, study of the mechanisms of CKD muscle atrophy has made substantial progress.…”

Section: Introductionmentioning

confidence: 99%

Formononetin ameliorates muscle atrophy by regulating myostatin‐mediated PI3K/Akt/FoxO3a pathway and satellite cell function in chronic kidney disease

Liu

You

et al. 2021

J Cellular Molecular Medi

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Muscle atrophy is a common complication in chronic kidney disease (CKD). Inflammation and myostatin play important roles in CKD muscle atrophy. Formononetin (FMN), which is a major bioactive isoflavone compound in Astragalus membranaceus , exerts anti‐inflammatory effects and the promotion of myogenic differentiation. Our study is based on myostatin to explore the effects and mechanisms of FMN in relation to CKD muscle atrophy. In this study, CKD rats and tumour necrosis factor α (TNF‐α)‐induced C2C12 myotubes were used for in vivo and in vitro models of muscle atrophy. The results showed that FMN significantly improved the renal function, nutritional status and inflammatory markers in CKD rats. Values for bodyweight, weight of tibialis anterior and gastrocnemius muscles, and cross‐sectional area (CSA) of skeletal muscles were significantly larger in the FMN treatment rats. Furthermore, FMN significantly suppressed the expressions of MuRF‐1, MAFbx and myostatin in the muscles of CKD rats and the TNF‐α‐induced C2C12 myotubes. Importantly, FMN significantly increased the phosphorylation of PI3K, Akt, and FoxO3a and the expressions of the myogenic proliferation and differentiation markers, myogenic differentiation factor D (MyoD) and myogenin in muscles of CKD rats and the C2C12 myotubes. Similar results were observed in TNF‐α‐induced C2C12 myotubes transfected with myostatin‐small interfering RNA (si‐myostatin). Notably, myostatin overexpression plasmid (myostatin OE) abolished the effect of FMN on the phosphorylation of the PI3K/Akt/FoxO3a pathway and the expressions of MyoD and myogenin. Our findings suggest that FMN ameliorates muscle atrophy related to myostatin‐mediated PI3K/Akt/FoxO3a pathway and satellite cell function.

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Multiple organ dysfunction - we must take a closer look at muscle wasting!

Cited by 2 publications

References 5 publications

Paeoniflorin Ameliorates Skeletal Muscle Atrophy in Chronic Kidney Disease via AMPK/SIRT1/PGC-1α-Mediated Oxidative Stress and Mitochondrial Dysfunction

Paeoniflorin Ameliorates Skeletal Muscle Atrophy in Chronic Kidney Disease via AMPK/SIRT1/PGC-1α-Mediated Oxidative Stress and Mitochondrial Dysfunction

Formononetin ameliorates muscle atrophy by regulating myostatin‐mediated PI3K/Akt/FoxO3a pathway and satellite cell function in chronic kidney disease

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