ArticleMedical science monitor : international medical journal of experimental and clinical research2020
The Protein Kinase R Inhibitor C16 Alleviates Sepsis-Induced Acute Kidney Injury Through Modulation of the NF-κB and NLR Family Pyrin Domain-Containing 3 (NLPR3) Pyroptosis Signal Pathways.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Drug repurposing of sophoridine for sepsis-induced organ injury: from in-depth analysis of a single agent to a multi-target therapeutic paradigm.Frontiers in pharmacology · 2026Review
- Crosstalk of regulated cell death pathways in sepsis-associated acute kidney injury: implications for therapy.Frontiers in cell and developmental biology · 2026Review
- S-nitrosoglutathione inhibits pyroptosis of kidney tubular epithelial cells in sepsis via the SIRT3/SOD2/mtROS signaling pathway.Renal failure · 2025Article
- Pyroptosis in sepsis-associated acute kidney injury: mechanisms and therapeutic perspectives.Critical care (London, England) · 2025Review
- Modulating the gut microbiota and inflammation is involved in the effect of diosgenin against diabetic nephropathy in rat.Frontiers in pharmacology · 2025Article
- Pyroptosis: The Determinator of Cell Death and Fate in Acute Kidney Injury.Kidney diseases (Basel, Switzerland) · 2024Review
- Irisin Alleviates Cognitive Impairment by Inhibiting AhR/NF-Mediators of inflammation · 2024Article
- The role of inflammatory response and metabolic reprogramming in sepsis-associated acute kidney injury: mechanistic insights and therapeutic potential.Frontiers in immunology · 2024Review
- Protective Effects of Baicalein on Lipopolysaccharide-Induced AR42J PACs through Attenuation of Both Inflammation and Pyroptosis via Downregulation of miR-224-5p/PARP1.Mediators of inflammation · 2024Article
- The Role of Pyroptosis in the Pathogenesis of Kidney Diseases.Kidney diseases (Basel, Switzerland) · 2023Review
- CHIP protects against septic acute kidney injury by inhibiting NLRP3-mediated pyroptosis.iScience · 2023Article
- Tanshinone IIA inhibits cardiomyocyte pyroptosis through TLR4/NF-κB p65 pathway after acute myocardial infarction.Frontiers in cell and developmental biology · 2023Article
- Identifying Candidate Protein Markers of Acute Kidney Injury in Acute Decompensated Heart Failure.International journal of molecular sciences · 2022Article
- The "Self-Sacrifice" of ImmuneCells in Sepsis.Frontiers in immunology · 2022Review
- Protein Kinase R in Bacterial Infections: Friend or Foe?Frontiers in immunology · 2021Review
- The Programmed Cell Death of Macrophages, Endothelial Cells, and Tubular Epithelial Cells in Sepsis-AKI.Frontiers in medicine · 2021Review
- Angiotensin (1-7) Attenuates Sepsis-Induced Acute Kidney Injury by Regulating the NF-κB Pathway.Frontiers in pharmacology · 2021Article
- Long Non-coding RNAFrontiers in physiology · 2021Article
- Interferon-Stimulated Genes: Novel Targets in Renal Pathogenesis.Kidney diseases (Basel, Switzerland)Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Protein kinase R (PKR) is implicated in the inflammatory response to bacterial infection while the role of PKR in sepsis-induced acute kidney injury (AKI) is largely unknown. This study aimed to investigate the effects of the specific PKR inhibitor C16 (C13H8N4OS) on lipopolysaccharide (LPS)-induced AKI, and its mechanisms of action. MATERIAL AND METHODS C57BL/6J mice were injected intraperitoneally with C16 or vehicle 1 h before the LPS challenge and then injected intraperitoneally with LPS or 0.9% saline. After the LPS challenge, histopathological damage, renal function, and levels of proinflammatory cytokines were assessed. All the related signaling pathways were analyzed. RESULTS C16 effectively inhibited LPS-induced renal elevation of proinflammatory cytokines and chemokines. C16 prevented NF-kappaB activation and suppressed the PKR/eIF2alpha signaling pathway in AKI after the LPS challenge. Furthermore, C16 significantly inhibited pyroptosis during AKI, as evidenced by decreased renal levels of apoptosis-associated speck-like protein; NACHT, LRR, NLR Family Pyrin Domain-Containing 3; caspase-1; interleukin (IL)-1ß; and IL-18. CONCLUSIONS Our findings suggest that inhibition by C16 ameliorated LPS-induced renal inflammation and injury, at least partly through modulation of the pyroptosis signal pathway in the kidney.
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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.