ArticleJournal of the American Society of Nephrology : JASN2011
Decreased miR-29 suppresses myogenesis in CKD.
Article in Journal of the American Society of Nephrology : JASN, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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Who cites it
68 citing papers in PubMed.
- The Role of Extracellular Vesicles in Musculoskeletal Diseases.Journal of extracellular vesicles · 2025Review
- Renin angiotensin system-induced muscle wasting: putative mechanisms and implications for clinicians.Molecular and cellular biochemistry · 2025Review
- Combating chronic kidney disease-associated cachexia: A literature review of recent therapeutic approaches.BMC nephrology · 2025Review
- Sarcopenia in Chronic Kidney Disease: A Narrative Review from Pathophysiology to Therapeutic Approaches.Biomedicines · 2025Review
- Hypermethylation and suppression of microRNA219a-2 activates the ALDH1L2/GSH/PAI-1 pathway for fibronectin degradation in renal fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Hochuekkito accelerates recovery from cisplatin induced-muscle atrophy accompanied by slow-twitch fiber-specific microRNA upregulation in mice.Frontiers in pharmacology · 2025Article
- Circulating Muscle Markers for Sarcopenia in Peritoneal Dialysis.International journal of nephrology · 2025Review
- MiR-126 accelerates renal injury induced by UUO via inhibition PI3K/ IRS-1/ FAK signaling induced M2 polarization and endocytosis in macrophages.Scientific reports · 2024Article
- Pathogenesis of Sarcopenia in Chronic Kidney Disease-The Role of Inflammation, Metabolic Dysregulation, Gut Dysbiosis, and microRNA.International journal of molecular sciences · 2024Review
- Extracellular MicroRNAs as Potential Biomarkers for Frail Kidney Phenotype: Progresses and Precautions.Aging and disease · 2024Article
- Epigenetics of Skeletal Muscle Atrophy.International journal of molecular sciences · 2024Review
- HucMSCs Delay Muscle Atrophy After Peripheral Nerve Injury Through Exosomes by Repressing Muscle-Specific Ubiquitin Ligases.Stem cells (Dayton, Ohio) · 2024Article
- Article
- The Impact of Physical Exercise on microRNAs in Hemodialysis Patients: A Review and a Protocol for an Ancillary Study.Biomedicines · 2024Review
- Muscle Wasting in Chronic Kidney Disease: Mechanism and Clinical Implications-A Narrative Review.International journal of molecular sciences · 2022Review
- Micro-RNAs: A safety net to protect hematopoietic stem cell self-renewal.Wiley interdisciplinary reviews. RNA · 2022Review
- Primary skeletal muscle cells from chronic kidney disease patients retain hallmarks of cachexia in vitro.Journal of cachexia, sarcopenia and muscle · 2022Article
- Pathophysiological mechanisms leading to muscle loss in chronic kidney disease.Nature reviews. Nephrology · 2022Review
- Role of exosomes and exosomal microRNA in muscle-Kidney crosstalk in chronic kidney disease.Frontiers in cell and developmental biology · 2022Review
- Klotho/FGF23 and Wnt in SHPT associated with CKDAmerican journal of translational research · 2022Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
The mechanisms underlying the muscle wasting that accompanies CKD are not well understood. Animal models suggest that impaired differentiation of muscle progenitor cells may contribute. Expression of the myogenesis-suppressing transcription factor Ying Yang-1 increases in muscle of animals with CKD, but the mechanism underlying this increased expression is unknown. Here, we examined a profile of microRNAs in muscles from mice with CKD and observed downregulation of both microRNA-29a (miR-29a) and miR-29b. Because miR-29 has a complementary sequence to the 3'-untranslated region of Ying Yang-1 mRNA, a decrease in miR-29 could increase Ying Yang-1. We used adenovirus-mediated gene transfer to express miR-29 in C2C12 myoblasts and measured its effect on both Ying Yang-1 and myoblast differentiation. An increase in miR-29 decreased the abundance of Ying Yang-1 and improved the differentiation of myoblasts into myotubes. Similarly, using myoblasts isolated from muscles of mice with CKD, an increase in miR-29 improved differentiation of muscle progenitor cells into myotubes. In conclusion, CKD suppresses miR-29 in muscle, which leads to higher expression of the transcription factor Ying Yang-1, thereby suppressing myogenesis. These data suggest a potential mechanism for the impaired muscle cell differentiation associated with CKD.
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