ArticleRedox biology2018
Oxalate induces mitochondrial dysfunction and disrupts redox homeostasis in a human monocyte derived cell line.
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, 1 of them a synthesis that pooled it.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Metabolic changes in kidney stone disease.Frontiers in immunology · 2023Pooled it
- Cell type-stratified immunogenetic framework reveals immune drivers and therapeutic targets in kidney stone disease.Molecular therapy. Nucleic acids · 2026Article
- Host immunosenescence compromisesAging · 2026Article
- Oxalate as an Emerging Contributor to Cardiovascular Disease: Links to Inflammation, Immunity, and Oxidative Stress.Nutrients · 2026Review
- Oxalate induces proliferation and mitochondrial metabolism in select clear cell renal cell carcinoma cell lines.BMC cancer · 2026Article
- Systematic proteomics analysis of lysine acetylation reveals critical features of renal proteins in kidney calculi formation.PloS one · 2026Article
- Genetically predicted blood metabolites mediate the association between immune cell characteristics and urolithiasis: A Mendelian randomization study and mediation analysis.Genes & diseases · 2025Article
- Macrophage Reprogramming: Emerging Molecular Therapeutic Strategies for Nephrolithiasis.Biomolecules · 2025Review
- Colonization withbioRxiv : the preprint server for biology · 2025Article
- GOLPH3 promotes calcium oxalate-induced renal injury and fibrosis through Golgi stress-mediated apoptosis and inflammatory responses.Scientific reports · 2025Article
- Article
- Association between the systemic inflammation response index and kidney stones in US adults: a cross-sectional study based on NHANES 2007-2018.Urolithiasis · 2024Article
- Integrative bioinformatics analysis for identifying the mitochondrial-related gene signature associated with immune infiltration in premature ovarian insufficiency.BMC medicine · 2024Article
- Inhibition of hepatic oxalate overproduction ameliorates metabolic dysfunction-associated steatohepatitis.Nature metabolism · 2024Article
- Abnormal Porphyrin Metabolism in Autism Spectrum Disorder and Therapeutic Implications.Molecular neurobiology · 2024Review
- Understanding formation processes of calcareous nephrolithiasis in renal interstitium and tubule lumen.Journal of cellular and molecular medicine · 2024Review
- The association between C-reactive protein levels and the risk of kidney stones: a population-based study.BMC nephrology · 2024Article
- Different Degrees of Sulfated Laminaria Polysaccharides Recovered Damaged HK-2 Cells and Inhibited Adhesion of Nano-COM and Nano-COD Crystals.Bioinorganic chemistry and applications · 2024Article
- Hydroxycitric acid prevents hyperoxaluric-induced nephrolithiasis and oxidative stress via activation of the Nrf2/Keap1 signaling pathway.Cell cycle (Georgetown, Tex.) · 2023Article
- Oxalate (dys)Metabolism: Person-to-Person Variability, Kidney and Cardiometabolic Toxicity.Genes · 2023Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Monocytes/macrophages are thought to be recruited to the renal interstitium during calcium oxalate (CaOx) kidney stone disease for crystal clearance. Mitochondria play an important role in monocyte function during the immune response. We recently determined that monocytes in patients with CaOx kidney stones have decreased mitochondrial function compared to healthy subjects. The objective of this study was to determine whether oxalate, a major constituent found in CaOx kidney stones, alters cell viability, mitochondrial function, and redox homeostasis in THP-1 cells, a human derived monocyte cell line. THP-1 cells were treated with varying concentrations of CaOx crystals (insoluble form) or sodium oxalate (NaOx; soluble form) for 24h. In addition, the effect of calcium phosphate (CaP) and cystine crystals was tested. CaOx crystals decreased cell viability and induced mitochondrial dysfunction and redox imbalance in THP-1 cells compared to control cells. However, NaOx only caused mitochondrial damage and redox imbalance in THP-1 cells. In contrast, both CaP and cystine crystals did not affect THP-1 cells. Separate experiments showed that elevated oxalate also induced mitochondrial dysfunction in primary monocytes from healthy subjects. These findings suggest that oxalate may play an important role in monocyte mitochondrial dysfunction in CaOx kidney stone disease.
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Registered trials
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