ArticleNutrition (Burbank, Los Angeles County, Calif.)2023
Polyunsaturated fatty acids ameliorate renal stone-induced renal tubular damage via miR-93-5p/Pknox1 axis.
Article in Nutrition (Burbank, Los Angeles County, Calif.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Unravelling new mechanisms of occurrence and recurrence in calcium nephrolithiasis: the role of epigenetics.World journal of urology · 2026Review
- Linoelaidic acid alleviates COM-induced kidney injury and crystal deposition via the PPARγ/MAPK signaling pathway.Urolithiasis · 2025Article
- Gut microbiota-derived indole-3-acetic acid ameliorates calcium oxalate renal stone formation via AHR/NF‑κB axis.Urolithiasis · 2025Article
- Planetary Health Diet Index and self-reported kidney stones in US adults: mediating role of high-density lipoprotein cholesterol.Frontiers in nutrition · 2025Article
- Inhibiting miRNA-146a suppresses mouse gallstone formation by regulating LXR/megalin/cubilin-media cholesterol absorption.Heliyon · 2024Article
- Cell death‑related molecules and targets in the progression of urolithiasis (Review).International journal of molecular medicine · 2024Review
- Non-Coding RNAs in Kidney Stones.Biomolecules · 2024Review
- METTL14 drives growth and metastasis of non-small cell lung cancer by regulating pri-miR-93-5p maturation and TXNIP expression.Genes & genomics · 2024Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesPolyunsaturated fatty acids (PUFAs) can decrease the risk of calcium oxalate stone formation, which accounts for 80% of all renal stones. This study aimed to investigate the protective mechanisms of PUFAs against renal stones.
methodsUrine samples of patients with renal stones and biopsy tissue samples from patients with nephrocalcinosis were tested for miR-93-5p expression. A renal stone mouse model was established with intraperitoneal injection of glyoxylic acid, during which mice were treated with PUFAs and/or an miR-93-5p inhibitor adenovirus. Periodic acid-Schiff staining, terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling staining, oil red O staining, triacylglycerol assay, and colorimetry testing were performed to assess glycogen deposition, apoptosis, lipid accumulation, blood urea nitrogen, and serum creatinine levels, respectively. Renal proximal tubular epithelial cells (human kidney 2 [HK-2]) were subjected to gain- and loss-of-function assays before calcium-oxalate monohydrate (COM) induction and PUFA treatment. Cell counting kit 8, flow cytometry, and lactate dehydrogenase activity assays were used to examine cell viability, apoptosis, and damage. A luciferase reporter gene assay verified the interaction between miR-93-5p and Pknox1, and miR-93-5p and Pknox1 levels were assessed using a reverse transcription-quantitative polymerase chain reaction and Western blot analysis.
resultsmiR-93-5p was downregulated in clinical samples with renal stones and negatively targeted Pknox1. PUFAs increased miR-93-5p expression and reduced apoptosis, glycogen deposition, and lipid accumulation in mice with renal stones, which were annulled by miR-93-5p downregulation. PUFAs increased proliferation and diminished apoptosis, lipid accumulation, and lactate dehydrogenase activity in COM-induced HK-2 cells, which were negated by miR-93-5p inhibition. Pknox1 overexpression reversed the effect of miR-93-5p upregulation on COM-induced HK-2 cells.
conclusionsPUFAs repressed renal stone-induced renal tubular damage via the miR-93-5p/Pknox1 axis.
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