scholarly journals Mechanisms of muscle wasting in chronic kidney disease

2014 ◽  
Vol 10 (9) ◽  
pp. 504-516 ◽  
Author(s):  
Xiaonan H. Wang ◽  
William E. Mitch
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Muscle Wasting

scholarly journals Indoxyl-Sulfate-Induced Redox Imbalance in Chronic Kidney Disease

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 936
Author(s):  
Chien-Lin Lu ◽  
Cai-Mei Zheng ◽  
Kuo-Cheng Lu ◽  
Min-Tser Liao ◽  
Kun-Lin Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Muscle Wasting ◽  
Mesangial Cells ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Indoxyl Sulfate ◽  
Uremic Toxin ◽  
Tubulointerstitial Injury

The accumulation of the uremic toxin indoxyl sulfate (IS) induces target organ damage in chronic kidney disease (CKD) patients, and causes complications including cardiovascular diseases, renal osteodystrophy, muscle wasting, and anemia. IS stimulates reactive oxygen species (ROS) production in CKD, which impairs glomerular filtration by a direct cytotoxic effect on the mesangial cells. IS further reduces antioxidant capacity in renal proximal tubular cells and contributes to tubulointerstitial injury. IS-induced ROS formation triggers the switching of vascular smooth muscular cells to the osteoblastic phenotype, which induces cardiovascular risk. Low-turnover bone disease seen in early CKD relies on the inhibitory effects of IS on osteoblast viability and differentiation, and osteoblastic signaling via the parathyroid hormone. Excessive ROS and inflammatory cytokine releases caused by IS directly inhibit myocyte growth in muscle wasting via myokines’ effects. Moreover, IS triggers eryptosis via ROS-mediated oxidative stress, and elevates hepcidin levels in order to prevent iron flux in circulation in renal anemia. Thus, IS-induced oxidative stress underlies the mechanisms in CKD-related complications. This review summarizes the underlying mechanisms of how IS mediates oxidative stress in the pathogenesis of CKD’s complications. Furthermore, we also discuss the potential role of oral AST-120 in attenuating IS-mediated oxidative stress after gastrointestinal adsorption of the IS precursor indole.

scholarly journals Long-noncoding RNA Atrolnc-1 promotes muscle wasting in mice with chronic kidney disease

2018 ◽  
Vol 9 (5) ◽  
pp. 962-974 ◽  
Author(s):  
Lijing Sun ◽  
Meijun Si ◽  
Xinyan Liu ◽  
Jong Min Choi ◽  
Yanlin Wang ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Muscle Wasting

scholarly journals Atractylenolide III Attenuates Muscle Wasting in Chronic Kidney Disease via the Oxidative Stress-Mediated PI3K/AKT/mTOR Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-16 ◽  
Author(s):  
Mingqing Wang ◽  
Rong Hu ◽  
Yanjing Wang ◽  
Lingyu Liu ◽  
Haiyan You ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Skeletal Muscles ◽  
Muscle Wasting ◽  
Mtor Pathway ◽  
C2c12 Myoblast ◽  
Model Group ◽  
Atractylenolide Iii

Oxidative stress contributes to muscle wasting in advanced chronic kidney disease (CKD) patients. Atractylenolide III (ATL-III), the major active constituent of Atractylodes rhizome, has been previously reported to function as an antioxidant. This study is aimed at investigating whether ATL-III has protective effects against CKD-induced muscle wasting by alleviating oxidative stress. The results showed that the levels of serum creatinine (SCr), blood urea nitrogen (BUN), and urinary protein significantly decreased in the ATL-III treatment group compared with the 5/6 nephrectomy (5/6 Nx) model group but were higher than those in the sham operation group. Skeletal muscle weight was increased, while inflammation was alleviated in the ATL-III administration group compared with the 5/6 Nx model group. ATL-III-treated rats also showed reduced dilation of the mitochondria, increased CAT, GSH-Px, and SOD activity, and decreased levels of MDA both in skeletal muscles and serum compared with 5/6 Nx model rats, suggesting that ATL-III alleviated mitochondrial damage and increased the activity of antioxidant enzymes, thus reducing the production of ROS. Furthermore, accumulated autophagosomes (APs) and autolysosomes (ALs) were reduced in the gastrocnemius (Gastroc) muscles of ATL-III-treated rats under transmission electron microscopy (TEM) together with the downregulation of LC3-II and upregulation of p62 according to Western blotting. This evidence indicated that ATL-III improved skeletal muscle atrophy and alleviated oxidative stress and autophagy in CKD rats. Furthermore, ATL-III could also increase the protein levels of p-PI3K, p-AKT, and p-mTOR in skeletal muscles in CKD rats. To further reveal the relevant mechanism, the oxidative stress-mediated PI3K/AKT/mTOR pathway was assessed, which showed that a reduced expression of p-PI3K, p-AKT, and p-mTOR in C2C12 myoblast atrophy induced by TNF-α could be upregulated by ATL-III; however, after the overexpression of Nox2 to increase ROS production, the attenuated effect was reversed. Our findings indicated that ATL-III is a potentially protective drug against muscle wasting via activation of the oxidative stress-mediated PI3K/AKT/mTOR pathway.

scholarly journals Suppression of muscle wasting by the plant-derived compound ursolic acid in a model of chronic kidney disease

2016 ◽  
Vol 8 (2) ◽  
pp. 327-341 ◽  
Author(s):  
Rizhen Yu ◽  
Ji-an Chen ◽  
Jing Xu ◽  
Jin Cao ◽  
Yanlin Wang ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Ursolic Acid ◽  
Muscle Wasting

scholarly journals Maintenance of Skeletal Muscle to Counteract Sarcopenia in Patients with Advanced Chronic Kidney Disease and Especially Those Undergoing Hemodialysis

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1538
Author(s):  
Katsuhito Mori
Keyword(s):  
Skeletal Muscle ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Muscle Wasting ◽  
Modern Society ◽  
Life Extension ◽  
Muscle Physiology ◽  
Protein Energy Wasting ◽  
Protein Energy ◽  
New Concepts

Life extension in modern society has introduced new concepts regarding such disorders as frailty and sarcopenia, which has been recognized in various studies. At the same time, cutting-edge technology methods, e.g., renal replacement therapy for conditions such as hemodialysis (HD), have made it possible to protect patients from advanced lethal chronic kidney disease (CKD). Loss of muscle and fat mass, termed protein energy wasting (PEW), has been recognized as prognostic factor and, along with the increasing rate of HD introduction in elderly individuals in Japan, appropriate countermeasures are necessary. Although their origins differ, frailty, sarcopenia, and PEW share common components, among which skeletal muscle plays a central role in their etiologies. The nearest concept may be sarcopenia, for which diagnosis techniques have recently been reported. The focus of this review is on maintenance of skeletal muscle against aging and CKD/HD, based on muscle physiology and pathology. Clinically relevant and topical factors related to muscle wasting including sarcopenia, such as vitamin D, myostatin, insulin (related to diabetes), insulin-like growth factor I, mitochondria, and physical inactivity, are discussed. Findings presented thus far indicate that in addition to modulation of the aforementioned factors, exercise combined with nutritional supplementation may be a useful approach to overcome muscle wasting and sarcopenia in elderly patients undergoing HD treatments.

scholarly journals Screening for muscle wasting and dysfunction in patients with chronic kidney disease

2016 ◽  
Vol 90 (1) ◽  
pp. 53-66 ◽  
Author(s):  
Juan J. Carrero ◽  
Kirsten L. Johansen ◽  
Bengt Lindholm ◽  
Peter Stenvinkel ◽  
Lilian Cuppari ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Muscle Wasting

Muscle wasting in hospitalized patients with chronic kidney disease in a non-dialysis phase

2021 ◽  
Vol 46 ◽  
pp. S610-S611
Author(s):  
R.L. Ferretti ◽  
F. Navarro ◽  
T.F. de Jesus ◽  
T. Moliterno ◽  
M. Menecucci
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Muscle Wasting ◽  
Hospitalized Patients

scholarly journals The nuclear phosphatase SCP4 regulates FoxO transcription factors during muscle wasting in chronic kidney disease

2017 ◽  
Vol 92 (2) ◽  
pp. 336-348 ◽  
Author(s):  
Xinyan Liu ◽  
Rizhen Yu ◽  
Lijing Sun ◽  
Giacomo Garibotto ◽  
Xia Lin ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Transcription Factors ◽  
Kidney Disease ◽  
Muscle Wasting ◽  
Foxo Transcription Factors
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