ArticleCellular and molecular life sciences : CMLS2024
miR-148b-5p regulates hypercalciuria and calcium-containing nephrolithiasis.
Article in Cellular and molecular life sciences : CMLS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Cross-Species Identification of Urinary Small Extracellular Vesicle-Associated miR-223-3p as a Candidate Biomarker for Nephrolithiasis in a Discovery Cohort.International journal of medical sciences · 2026Article
- Linoelaidic acid alleviates COM-induced kidney injury and crystal deposition via the PPARγ/MAPK signaling pathway.Urolithiasis · 2025Article
- Selected miRNAs in Urinary Extracellular Vesicles Show Promise for Early and Specific Diagnostics of Diabetic Kidney Disease.Journal of extracellular biology · 2025Article
- CREB1/CRTC2 regulated tubular epithelial-derived exosomal miR-93-3p promotes kidney injury induced by calcium oxalate via activating M1 polarization and macrophage extracellular trap formation.Journal of nanobiotechnology · 2025Article
- Regulating the balance between GSDMD-mediated pyroptosis and CHMP4B-dependent cell repair attenuates calcium oxalate kidney stone formation.International journal of biological sciences · 2025Article
- miR-574-5p in epigenetic regulation and Toll-like receptor signaling.Cell communication and signaling : CCS · 2024Review
- Noncoding RNA, friend or foe for nephrolithiasis?Frontiers in cell and developmental biology · 2024Review
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Authors and funding
17 authors.
Funding
Abstract
Calcium-containing stones represent the most common form of kidney calculi, frequently linked to idiopathic hypercalciuria, though their precise pathogenesis remains elusive. This research aimed to elucidate the molecular mechanisms involved by employing urinary exosomal microRNAs as proxies for renal tissue analysis. Elevated miR-148b-5p levels were observed in exosomes derived from patients with kidney stones. Systemic administration of miR-148b-5p in rat models resulted in heightened urinary calcium excretion, whereas its inhibition reduced stone formation. RNA immunoprecipitation combined with deep sequencing identified miR-148b-5p as a suppressor of calcitonin receptor (Calcr) expression, thereby promoting urinary calcium excretion and stone formation. Mice deficient in Calcr in distal epithelial cells demonstrated elevated urinary calcium excretion and renal calcification. Mechanistically, miR-148b-5p regulated Calcr through the circRNA-83536/miR-24-3p signaling pathway. Human kidney tissue samples corroborated these results. In summary, miR-148b-5p regulates the formation of calcium-containing kidney stones via the circRNA-83536/miR-24-3p/Calcr axis, presenting a potential target for novel therapeutic interventions to prevent calcium nephrolithiasis.
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