Sarcopenia in Chronic Kidney Disease: Factors, Mechanisms, and Therapeutic Interventions
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- Watanabe Hiroshi
- Department of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Kumamoto University
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- Enoki Yuki
- Division of Pharmacodynamics, Keio University Faculty of Pharmacy
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- Maruyama Toru
- Department of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Kumamoto University
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<p>Chronic kidney disease (CKD), a chronic catabolic condition, is characterized by muscle wasting and decreased muscle endurance. Many insights into the molecular mechanisms of muscle wasting in CKD have been obtained. A persistent imbalance between protein degradation and synthesis in muscle causes muscle wasting. During muscle wasting, high levels of reactive oxygen species (ROS) and inflammatory cytokines are detected in muscle. These increased ROS and inflammatory cytokine levels induce the expression of myostatin. The myostatin binding to its receptor activin A receptor type IIB stimulates the expression of atrogenes such as atrogin-1 and muscle ring factor 1, members of the muscle-specific ubiquitin ligase family. Impaired mitochondrial function also contributes to reducing muscle endurance. The increased protein-bound uremic toxin, parathyroid hormone, glucocorticoid, and angiotensin II levels that are observed in CKD all have a negative effect on muscle mass and endurance. Among the protein-bound uremic toxins, indoxyl sulfate, an indole-containing compound has the potential to induce muscle atrophy by stimulating ROS-mediated myostatin and atrogenes expression. Indoxyl sulfate also impairs mitochondrial function. Some potential therapeutic approaches based on the muscle wasting mechanisms in CKD are currently in the testing stages.</p>
収録刊行物
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- Biological & Pharmaceutical Bulletin
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Biological & Pharmaceutical Bulletin 42 (9), 1437-1445, 2019-09-01
公益社団法人 日本薬学会
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詳細情報 詳細情報について
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- CRID
- 1390001277344399744
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- NII論文ID
- 130007700086
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- NII書誌ID
- AA10885497
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- ISSN
- 13475215
- 09186158
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- NDL書誌ID
- 029920355
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- PubMed
- 31474705
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
- KAKEN
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- 使用不可