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Remdesivir Alleviates Acute Kidney Injury by Inhibiting the Activation of NLRP3 Inflammasome
Liang Yin1,2, Haoxin Zhao3, Huiyu Zhang4
1Department of Central Laboratory, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Abstract:
Acute kidney injury (AKI) is a frequent clinical complication in critically ill patients, and it rapidly develops into renal failure with high morbidity and mortality. However, other than dialysis, no effective therapeutic interventions can offer reliable treatment to limit renal injury and improve survival. Here, we firstly reported that remdesivir (RDV, GS-5734), a broad-spectrum antiviral nucleotide prodrug, alleviated AKI by specifically inhibiting NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome activation in macrophages. Mechanically, RDV effectively suppressed the activities of nuclear transcription factor (NF)-κB, mitogen-activated protein kinase (MAPK), which further led to the reduction of the inflammasome genes of NLRP3 transcription, limiting the activation of NLRP3 inflammasome in vivo and in vitro. RDV also inhibited other pro-inflammatory genes including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-12, IL-1β, and interferon-β (IFN-β), leading to the reduction of inflammatory factors release. Thus, RDV can ameliorate AKI via modulating macrophage inflammasome activation and inflammatory immune responses and may have a therapeutic potential for patients with AKI in clinical application.
Insights
Remdesivir alleviates acute kidney injury (AKI) by inhibiting the NLRP3 inflammasome in macrophages. This antiviral drug reduces inflammation and may offer a new therapeutic option for AKI patients.
Area of Science:
- Immunology
- Nephrology
- Pharmacology
Background:
- Acute kidney injury (AKI) is a common complication in critically ill patients, often leading to renal failure with high mortality.
- Current treatments for AKI are limited, with dialysis being the primary intervention, highlighting the need for novel therapeutic strategies.
Purpose of the Study:
- To investigate the potential of remdesivir (RDV) as a therapeutic agent for AKI.
- To elucidate the mechanism by which RDV may alleviate AKI, focusing on inflammasome activation in macrophages.
Main Methods:
- Utilized both in vivo and in vitro models to assess the effects of RDV on AKI.
- Examined the impact of RDV on NLRP3 inflammasome activation, NF-κB and MAPK signaling pathways, and the expression of pro-inflammatory cytokines.
Main Results:
- Remdesivir (RDV) demonstrated efficacy in ameliorating AKI.
- RDV specifically inhibited the activation of the NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome in macrophages.
- RDV suppressed NF-κB and MAPK signaling, reducing NLRP3 transcription and the release of pro-inflammatory cytokines like TNF-α, IL-6, and IL-1β.
Conclusions:
- Remdesivir ameliorates AKI by modulating macrophage inflammasome activation and inflammatory responses.
- RDV exhibits therapeutic potential for AKI patients by targeting key inflammatory pathways.
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