ArticleFrontiers in pharmacology2022
Cpd-42 protects against calcium oxalate nephrocalcinosis-induced renal injury and inflammation by targeting RIPK3-mediated necroptosis.
Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 19 citations in OpenAlex.
- A Rare RIPK3 Variant Enhances Necroptosis and Promotes Inflammation in a Still Disease-Like Autoinflammatory Syndrome.Arthritis & rheumatology (Hoboken, N.J.) · 2026Article
- β-carotene attenuates calcium oxalate crystal-induced renal injury through suppression of NF-κB-mediated inflammation.Urolithiasis · 2026Article
- SIRT1 regulates CaOx crystal-induced exacerbation of renal mitochondrial dysfunction and fibrosis through PPAR-α in aged mice.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Review on the Mechanism of and Therapies Targeting PANoptosis in Ulcerative Colitis.Biomolecules · 2026Review
- CircRSPRY1 regulates calcium oxalate crystal-induced necrotic apoptosis in renal tubules via miR-21-5p/PTEN.Cell & bioscience · 2026Article
- A study based on reverse network pharmacology of kidney stones identified that quercetin targets the myosin light chain kinase/myosin light chain 2 pathway in human renal HK-2 cells.Asian journal of urology · 2026Article
- Review
- Salidroside attenuates calcium oxalate-induced renal injury via suppression of PANoptosis.Urolithiasis · 2026Article
- Regulated Cell Death in Calcium Oxalate Stone Disease: From Tubular Epithelial Injury to Inflammatory Amplification.Journal of inflammation research · 2026Review
- GGT1 protects against calcium oxalate crystal-induced renal tubular epithelial cell injury by targeting GCLC.Urolithiasis · 2025Article
- Hydrogen Sulfide Deficiency Contributes to Tubular Damage and Calcium Oxalate Crystal Formation in Hyperoxaluria Nephropathy: Role of Osteopontin and Tamm-Horsfall Protein.Antioxidants (Basel, Switzerland) · 2025Article
- Klotho alleviates oxidative stress and mitochondrial dysfunction through the Nrf2/HO-1 pathway, thereby reducing renal senescence induced by calcium oxalate crystals.Urolithiasis · 2025Article
- Cell death‑related molecules and targets in the progression of urolithiasis (Review).International journal of molecular medicine · 2024Review
- RIPK3 signaling and its role in regulated cell death and diseases.Cell death discovery · 2024Review
- Molecular mechanism of Rhizoma Polygonati in the treatment of nephrolithiasis: network pharmacology analysis and in vivo experimental verification.Urolithiasis · 2024Article
- Article
- Mechanisms of PANoptosis and relevant small-molecule compounds for fighting diseases.Cell death & disease · 2023Review
- Proteomic and computational analyses followed by functional validation of protective effects of trigonelline against calcium oxalate-induced renal cell deteriorations.Computational and structural biotechnology journal · 2023Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calcium oxalate (CaOx) crystals, as the predominant component of human kidney stones, can trigger excessive cell death and inflammation of renal tubular epithelial cells, involved in the pathogenesis of nephrocalcinosis. Necroptosis mediated by receptor-interacting protein kinase 3 (RIPK3) serves a critical role in the cytotoxicity of CaOx crystals. Here, we assessed the therapeutic potential of a novel RIPK3 inhibitor, compound 42 (Cpd-42), for CaOx nephrocalcinosis by comparison with dabrafenib, a classic RIPK3 inhibitor. Our results demonstrated that Cpd-42 pretreatment attenuated CaOx crystals-induced renal tubular epithelial cell (TEC) injury by inhibiting necroptosis and inflammation
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