ReviewFrontiers in immunology2026
Structural dynamics, pathogenic mechanisms, and therapeutic targeting of the NLRP3 inflammasome in lupus nephritis.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lupus nephritis (LN) is a severe complication of systemic lupus erythematosus (SLE). The nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome plays a central role in the pathogenesis of LN. Aberrant activation of the NLRP3 inflammasome directly promotes glomerular injury, proteinuria, and tubulointerstitial fibrosis through the induction of pyroptosis and the release of interleukin-1β (IL-1β) and IL-18. The expression level of the NLRP3 inflammasome is positively correlated with disease activity, making it both a key driver of acute renal injury in LN and a promising therapeutic target. In this review, a comprehensive summary of the structural features of NLRP3 is provided, including the pyrin domain (PYD), the nucleotide-binding oligomerization domain (NACHT), and the leucine-rich repeat domain (LRR). Additionally, the interaction between NIMA-related kinase 7 (NEK7) and the LRR domain is characterized, as well as the role of the fish-specific NACHT-associated (FISNA) domain in oligomerization. The canonical and non-canonical activation signaling pathways of the NLRP3 inflammasome are thoroughly analyzed. The pathological roles of the NLRP3 inflammasome in kidney-resident cells, including podocytes and renal tubular epithelial cells, as well as infiltrating immune cells, such as macrophages and T cells, are comprehensively discussed. Its crosstalk with multiple signaling pathways is also examined. Finally, the therapeutic potential of various intervention strategies, including direct inhibitors targeting NLRP3, upstream signaling pathway modulators, natural compounds, and novel gas therapies, in preclinical models of LN is evaluated. This review provides a comprehensive overview of the role of the NLRP3 inflammasome in LN and offers a theoretical basis for the development of novel NLRP3-targeted therapeutic strategies.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.