ArticleJournal of nanobiotechnology2026
Biomimetic hybrid nanoparticles for dual regulation of macrophage pyroptosis and metabolism in rheumatoid arthritis.
Article in Journal of nanobiotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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
1 citing paper in PubMed.
- RNA therapeutics in rheumatoid arthritis, systemic lupus erythematosus, and systemic sclerosis: a compartment-aware translational framework.Frontiers in immunology · 2026Review
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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
Rheumatoid arthritis (RA), a chronic and debilitating autoimmune inflammatory disease, is critically driven by macrophages within the inflamed synovium. The inflammatory cascade is sustained by a synergistic imbalance between macrophage pyroptosis and metabolic dysfunction, resulting in the formation of a dual barrier to effective intervention. GSDME-targeted siRNA delivery effectively blocks pyroptosis; however, uncorrected metabolic defects leave "saved" macrophages in a proinflammatory state, thereby aggravating RA. To address this "dual dilemma", folic acid-modified macrophage membrane-lipid hybrid nanoparticles (FA-MMLNPs) were engineered for spatiotemporally coordinated codelivery of GSDME siRNA (siG) and 4-octyl itaconate (4-OI). The biomimetic membrane promotes inflammatory homing, folic acid enhances FR-positive macrophage endocytosis, and the lipid core protects the siRNA and ensures synchronous release. Mechanistically, SiG inhibits pyroptosis, whereas 4-OI restores mitochondrial metabolism to reprogram macrophages to an anti-inflammatory phenotype. This integrated material platform organically combines pathway-specific gene silencing, metabolic correction, and precise biointerface engineering, providing a versatile paradigm for material design in RA and other inflammation-driven diseases.
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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.