ArticleAutophagy2020
Deregulated MTOR (mechanistic target of rapamycin kinase) is responsible for autophagy defects exacerbating kidney stone development.
Article in Autophagy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.
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Who cites it
34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 48 citations in OpenAlex.
- The role of autophagy in calcium oxalate kidney stone: A systematic review of the literature.Frontiers in physiology · 2022Pooled it
- Macrophage Function in Calcium Oxalate Kidney Stone Formation: A Systematic Review of Literature.Frontiers in immunology · 2021Pooled it
- Imbalance of renin-angiotensin system in calcium oxalate crystals-induced renal oxidative stress and autophagy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Article
- Unveiling potential natural promoters of calcium oxalate kidney stones in the urine via anion-exchange chromatography, crystal assays, and proteomics.Molecular and cellular biochemistry · 2026Article
- Calcium oxalate crystals exacerbate the damage and inflammation of renal tubular epithelial cells by blocking autophagic flux.Urolithiasis · 2026Article
- Oxalate induces proliferation and mitochondrial metabolism in select clear cell renal cell carcinoma cell lines.BMC cancer · 2026Article
- Apoptosis, ferroptosis, necrosis, necroptosis and pyroptosis in the formation of calcium oxalate kidney stones.Urolithiasis · 2025Review
- Sodium glucose co-transporter 2 inhibitor prevents nephrolithiasis in non-diabetes by restoring impaired autophagic flux.EBioMedicine · 2025Article
- Exploring the association between osteoporosis and kidney stones: a clinical to mechanistic translational study based on big data and bioinformatics.Biology direct · 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
- Prolyl hydroxylase domain inhibitors prevent kidney crystal formation by suppressing inflammation.Urolithiasis · 2024Article
- Linoleic Acid Enhances Renal Tubular Epithelial Cells Autophagy Caused by Calcium Oxalate Monohydrate Crystals.Journal of cellular and molecular medicine · 2024Article
- SMYD2 Promotes Calcium Oxalate-Induced Glycolysis in Renal Tubular Epithelial Cells via PTEN Methylation.Biomedicines · 2024Article
- The identification of key molecules and pathways in the crosstalk of calcium oxalate-treated TCMK-1 cells and macrophage via exosomes.Scientific reports · 2024Article
- Premature senescence is regulated by crosstalk among TFEB, the autophagy lysosomal pathway and ROS derived from damaged mitochondria in NaAsOCell death discovery · 2024Article
- A Membrane-Targeting Aggregation-Induced Emission Probe for Monitoring Lipid Droplet Dynamics in Ischemia/Reperfusion-Induced Cardiomyocyte Ferroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Nanotherapeutics targeting autophagy regulation for improved cancer therapy.Acta pharmaceutica Sinica. B · 2024Review
- N-acetylcysteine regulates oxalate induced injury of renal tubular epithelial cells through CDKN2B/TGF-β/SMAD axis.Urolithiasis · 2024Article
- Dysregulated palmitic acid metabolism promotes the formation of renal calcium-oxalate stones through ferroptosis induced by polyunsaturated fatty acids/phosphatidic acid.Cellular and molecular life sciences : CMLS · 2024Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kidney stone disease is a lifestyle-related disease prevalent in developed countries; however, effective medical treatment for the disease is not yet well established. As cellular damage in renal tubular cells (RTCs) is responsible for the disease, here, we focused on the role of macroautophagy/autophagy in RTCs. We found that autophagic activity was significantly decreased in mouse RTCs exposed to calcium oxalate (CaOx) monohydrate crystals and in the kidneys of GFP-conjugated MAP1LC3B (microtubule- associated protein 1 light chain 3 beta) transgenic mice with CaOx nephrocalcinosis induced by glyoxylate. This caused accumulation of damaged intracellular organelles, such as mitochondria and lysosomes, the normal functioning of which is mediated by functional autophagy. An impairment of autophagy was also observed in the mucosa with plaques of CaOx kidney stone formers. We determined that the decrease in autophagy was caused by an upregulation of MTOR (mechanistic target of rapamycin kinase), which consequently resulted in the suppression of the upstream autophagy regulator TFEB (transcription factor EB). Furthermore, we showed that an MTOR inhibitor could recover a decrease in autophagy and alleviate crystal-cell interactions and the formation of crystals associated with increased inflammatory responses. Taken together, we conclude that autophagy compromised by MTOR deregulation is a fundamental feature in the pathology of kidney stone formation, and propose that chemical inhibition of MTOR could be a prospective strategy for disease suppression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.