ArticleRedox biology2018
Autophagy inhibition attenuates hyperoxaluria-induced renal tubular oxidative injury and calcium oxalate crystal depositions in the rat kidney.
Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 2 of them syntheses that pooled it.
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Who cites it
44 citing papers in PubMed, 2 syntheses or guidelines pooled it, 89 citations in OpenAlex.
- The role of autophagy in calcium oxalate kidney stone: A systematic review of the literature.Frontiers in physiology · 2022Pooled it
- Role of ROS-Induced NLRP3 Inflammasome Activation in the Formation of Calcium Oxalate Nephrolithiasis.Frontiers in immunology · 2022Pooled it
- Gut Microbiota-Isoallolithocholic Acid Crosstalk Promotes Calcium Oxalate Kidney Stone Formation via PARP1-Mediated Parthanatos.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- EP3 receptor mediates calcium oxalate kidney stone formation via Ca²⁺/AKT and necroinflammation.Urolithiasis · 2026Article
- Calcium oxalate crystals exacerbate the damage and inflammation of renal tubular epithelial cells by blocking autophagic flux.Urolithiasis · 2026Article
- Total flavonoids ofFrontiers in pharmacology · 2026Article
- Sodium glucose co-transporter 2 inhibitor prevents nephrolithiasis in non-diabetes by restoring impaired autophagic flux.EBioMedicine · 2025Article
- Environmental determinants in the development of kidney stone.Urolithiasis · 2025Review
- Molecular insights into cell signaling pathways in kidney stone formation.Urolithiasis · 2025Review
- Regulating the balance between GSDMD-mediated pyroptosis and CHMP4B-dependent cell repair attenuates calcium oxalate kidney stone formation.International journal of biological sciences · 2025Article
- HACE1 as a bridge between oxidative stress and autophagy.Frontiers in immunology · 2025Review
- Single-Cell RNA Sequencing Analysis Reveals the Role of Macrophage-Mediated CD44-AKT-CCL2 Pathways in Renal Tubule Injury during Calcium Oxalate Crystal Formation.Research (Washington, D.C.) · 2025Article
- Decoding TMAO in the Gut-Organ Axis: From Biomarkers and Cell Death Mechanisms to Therapeutic Horizons.Drug design, development and therapy · 2025Review
- Sirtuin1 Suppresses Calcium Oxalate Nephropathy via Inhibition of Renal Proximal Tubular Cell Ferroptosis Through PGC-1α-mediated Transcriptional Coactivation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Linoleic Acid Enhances Renal Tubular Epithelial Cells Autophagy Caused by Calcium Oxalate Monohydrate Crystals.Journal of cellular and molecular medicine · 2024Article
- Mitochondrial dysfunction in kidney stones and relief of kidney stones after reducing mtROS.Urolithiasis · 2024Article
- Machine learning and 4D-LFQ quantitative proteomic analysis explore the molecular mechanism of kidney stone formation.Heliyon · 2024Article
- Cell death‑related molecules and targets in the progression of urolithiasis (Review).International journal of molecular medicine · 2024Review
- Long-Term Sodium Deficiency Reduces Sodium Excretion but Impairs Renal Function and Increases Stone Formation in Hyperoxaluric Calcium Oxalate Rats.International journal of molecular sciences · 2024Article
- Review
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperoxaluria-induced oxidative injury of renal tubular epithelial cell is a casual and essential factor in kidney calcium oxalate (CaOx) stone formation. Autophagy has been shown to be critical for the regulation of oxidative stress-induced renal tubular injury; however, little is known about its role in kidney CaOx stone formation. In the present study, we found that the autophagy antagonist chloroquine could significantly attenuate oxalate-induced autophagy activation, oxidative injury and mitochondrial damage of renal tubular cells in vitro and in vivo, as well as hyperoxaluria-induced CaOx crystals depositions in rat kidney, whereas the autophagy agonist rapamycin exerted contrasting effects. In addition, oxalate-induced p38 phosphorylation was significantly attenuated by chloroquine pretreatment but was markedly enhanced by rapamycin pretreatment, whereas the protective effect of chloroquine on rat renal tubular cell oxidative injury was partly reversed by a p38 protein kinase activator anisomycin. Furthermore, the knockdown of Beclin1 represented similar effects to chloroquine on oxalate-induced cell oxidative injury and p38 phosphorylation in vitro. Taken together, our results revealed that autophagy inhibition could attenuate oxalate-induced oxidative injury of renal tubular cell and CaOx crystal depositions in the rat kidney via, at least in part, inhibiting the activation of p38 signaling pathway, thus representing a novel role of autophagy in the regulation of oxalate-induced renal oxidative injury and CaOx crystal depositions for the first time.
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