ArticleJournal of cachexia, sarcopenia and muscle2023
The G protein-coupled receptor ligand apelin-13 ameliorates skeletal muscle atrophy induced by chronic kidney disease.
Article in Journal of cachexia, sarcopenia and muscle, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.
- Pooled it
- Microneedle patch-based delivery of Pyr-Apelin-13 reverses functional and structural deficits in age-related sarcopenia.Scientific reports · 2026Article
- Exercise-induced myokines in metabolic regulation: mechanisms, mimetics, and translational potential.Archives of pharmacal research · 2026Review
- APLNR reduction in kidney-muscle crosstalk in renal model recovered by exercise and STAT3 inhibition.Biochemistry and biophysics reports · 2026Article
- Dynamic monomer-dimer transition in ligand-induced apelin receptor activation.Nature communications · 2026Article
- Preventing Metabolic Syndrome in Adolescents Through Exercise.Advances in experimental medicine and biology · 2026Review
- Transcriptomic Insights Reveal PRTFDC1 as a Novel Regulator of Myogenic Differentiation in Sujiang Pig Satellite Cells.Veterinary sciences · 2025Article
- Article
- Apelin: A Promising Therapeutic Target for Degenerative Diseases of the Musculoskeletal System.Aging and disease · 2025Review
- miR-320-3p regulates apelin and TGF-β/SMAD3 signaling in hypobaric hypoxia exposed rats to induce skeletal muscle atrophy.Journal of physiology and biochemistry · 2025Article
- Liver B Cells Promotes MASLD Progression via the Apelin/APLNR System.International journal of medical sciences · 2025Article
- How Can Promoting Skeletal Muscle Health and Exercise in Children and Adolescents Prevent Insulin Resistance and Type 2 Diabetes?Life (Basel, Switzerland) · 2024Review
- Myokines: metabolic regulation in obesity and type 2 diabetes.Life metabolism · 2024Review
- Skeletal Muscle Injury in Chronic Kidney Disease-From Histologic Changes to Molecular Mechanisms and to Novel Therapies.International journal of molecular sciences · 2024Review
- Cysteine-cysteine Chemokine Receptor Type 5 Plays a Critical Role in Exercise Performance by Regulating Mitochondrial Content in Skeletal Muscle.Inflammation · 2023Article
- The G protein-coupled receptor ligand apelin-13 ameliorates skeletal muscle atrophy induced by chronic kidney disease.Journal of cachexia, sarcopenia and muscle · 2023Article
- Beneficial effects of Apelin-13 on metabolic diseases and exercise.Frontiers in endocrinology · 2023Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundTargeting of the apelin-apelin receptor (Apj) system may serve as a useful therapeutic intervention for the management of chronic kidney disease (CKD)-induced skeletal muscle atrophy. We investigated the roles and efficacy of the apelin-Apj system in CKD-induced skeletal muscle atrophy.
methodsThe 5/6-nephrectomized mice were used as CKD models. AST-120, a charcoal adsorbent of uraemic toxins (8 w/w% in diet), or apelin (1 μmol/kg) was administered to CKD mice to investigate the mechanism and therapeutic potential of apelin on CKD-induced skeletal muscle atrophy. The effect of indoxyl sulfate, a uraemic toxin, or apelin on skeletal muscle atrophy was evaluated using mouse myoblast cells (C2C12 cells) in vitro.
resultsSkeletal muscle atrophy developed over time following nephrectomy at 12 weeks, as confirmed by a significant increase of atrogin-1 and myostatin mRNA expression in the gastrocnemius (GA) muscle and a decrease of lower limb skeletal muscle weight (P < 0.05, 0.01 and 0.05, respectively). Apelin expression in GA muscle was significantly decreased (P < 0.05) and elabela, another Apj endogenous ligand, tended to show a non-significant decrease at 12 weeks after nephrectomy. Administration of AST-120 inhibited the decline of muscle weight and increase of atrogin-1 and myostatin expression. Apelin and elabela expression was slightly improved by AST-120 administration but Apj expression was not, suggesting the involvement of uraemic toxins in endogenous Apj ligand expression. The administration of apelin at 1.0 μmol/kg for 4 weeks to CKD mice suppressed the increase of atrogin-1 and myostatin, increased apelin and Apj mRNA expression at 30 min after apelin administration and significantly ameliorated weight loss and a decrease of the cross-sectional area of hindlimb skeletal muscle.
conclusionsThis study demonstrated for the first time the association of the Apj endogenous ligand-uraemic toxin axis with skeletal muscle atrophy in CKD and the utility of therapeutic targeting of the apelin-Apj system.
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