ArticleInternational journal of molecular sciences2020
Cyclophilin Inhibition Protects Against Experimental Acute Kidney Injury and Renal Interstitial Fibrosis.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 20 citations in OpenAlex.
- Mitochondrial dysfunction of renal tubular epithelial cells in chronic kidney disease-associated fibrosis: from organelle homeostasis to multicellular remodeling.Molecular biology reports · 2026Review
- Mechanism of Shoutai Wan against recurrent spontaneous abortion: regulation of decidual vascular remodeling via ERβ-ANGPT2 signaling axis.Functional & integrative genomics · 2026Article
- Acute Kidney Injury-to-Chronic Kidney Disease Transition-Associated Macrophage Subtypes: Biological Functions and Intercellular Crosstalk.International journal of molecular sciences · 2026Review
- Comprehensive analysis of CBL and CIPK gene families in Magnolia biondii and functional characterization of MbCBL4 under salt stress.Plant cell reports · 2026Article
- Divergent effects of semaglutide and CRV431 Co-therapy on liver fibrosis and HCC in MASLD mouse model.PloS one · 2026Article
- Innovative Insights into Interleukin-Mediated Macrophage Polarization: Metabolic Reprogramming and Inflammatory Pathway Crosstalk in Chronic Kidney Disease and Therapeutic Implications-A Narrative Review.International journal of general medicine · 2026Review
- Exploring diagnostic biomarkers of type 2 cardio-renal syndrome based on secreted proteins and bioinformatics analysis.Scientific reports · 2024Article
- Sanglifehrin A mitigates multiorgan fibrosis by targeting the collagen chaperone cyclophilin B.JCI insight · 2024Article
- Regulated cell death in chronic kidney disease: current evidence and future clinical perspectives.Frontiers in cell and developmental biology · 2024Review
- Research progress on the mechanism of renal interstitial fibrosis in obstructive nephropathy.Heliyon · 2023Review
- CC-4066 therapy delivered to kidneys during cold storage and assessed with normothermic reperfusion is feasible and safe.Frontiers in transplantation · 2023Article
- Inflammation in Health and Disease: New Insights and Therapeutic Avenues.International journal of molecular sciences · 2022Article
- Exploratory Investigation of the Plasma Proteome Associated with the Endotheliopathy of Trauma.International journal of molecular sciences · 2022Article
- Current update on theranostic roles of cyclophilin A in kidney diseases.Theranostics · 2022Review
- Article
- Proximal tubule cyclophilin D mediates kidney fibrogenesis in obstructive nephropathy.American journal of physiology. Renal physiology · 2021Article
- Cyclophilin D Promotes Acute, but Not Chronic, Kidney Injury in a Mouse Model of Aristolochic Acid Toxicity.Toxins · 2021Article
- An updated review on synthetic cathinones.Archives of toxicology · 2021Review
- Loss of endothelial glucocorticoid receptor promotes angiogenesis via upregulation of Wnt/β-catenin pathway.Angiogenesis · 2021Article
- In vivo toxicometabolomics reveals multi-organ and urine metabolic changes in mice upon acute exposure to human-relevant doses of 3,4-methylenedioxypyrovalerone (MDPV).Archives of toxicology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Cyclophilins have important homeostatic roles, but following tissue injury, cyclophilin A (CypA) can promote leukocyte recruitment and inflammation, while CypD can facilitate mitochondrial-dependent cell death. This study investigated the therapeutic potential of a selective cyclophilin inhibitor (GS-642362), which does not block calcineurin function, in mouse models of tubular cell necrosis and renal fibrosis. Mice underwent bilateral renal ischemia/reperfusion injury (IRI) and were killed 24 h later: treatment with 10 or 30 mg/kg/BID GS-642362 (or vehicle) began 1 h before surgery. In the second model, mice underwent unilateral ureteric obstruction (UUO) surgery and were killed 7 days later; treatment with 10 or 30 mg/kg/BID GS-642362 (or vehicle) began 1 h before surgery. GS-642362 treatment gave a profound and dose-dependent protection from acute renal failure in the IRI model. This protection was associated with reduced tubular cell death, including a dramatic reduction in neutrophil infiltration. In the UUO model, GS-642362 treatment significantly reduced tubular cell death, macrophage infiltration, and renal fibrosis. This protective effect was independent of the upregulation of IL-2 and activation of the stress-activated protein kinases (p38 and JNK). In conclusion, GS-642362 was effective in suppressing both acute kidney injury and renal fibrosis. These findings support further investigation of cyclophilin blockade in other types of acute and chronic kidney disease.
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