ArticleJournal of nanobiotechnology2026
Kidney‑enriched lipid nanoparticles delivering ANXA2 alleviate renal ischemia-reperfusion injury via CHMP2A-mediated necroptosis inhibition.
Article in Journal of nanobiotechnology, 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
12 authors.
Funding
Abstract
backgroundRenal ischemia-reperfusion injury (IRI) is a major complication following nephron-sparing surgery, with limited preventive strategies. Annexin A2 (ANXA2) is upregulated after renal IRI, but its functional role and therapeutic potential remain unclear.
methodsUtilizing ANXA2 knockout (KO) and wild-type mice subjected to renal IRI, we assessed injury, fibrosis, and cell death pathways. In vitro studies employed mouse renal tubular epithelial cells (TECs) with ANXA2 or charged multivesicular body protein (CHMP) 2A knockdown or overexpression. Molecular mechanisms were investigated via co-immunoprecipitation, mass spectrometry, and immunofluorescence. The Kidney-Targeting Peptide (KTP)-conjugated, ANXA2-loaded lipid nanoparticle (KTP-LNP@ANXA2) was synthesized and characterized. Its efficacy was evaluated in vitro and in a mouse renal IRI model.
resultsANXA2 was significantly upregulated post-IRI, predominantly in the renal medulla. KO mice exhibited exacerbated medullary injury, increased fibrosis, and enhanced necroptosis, as indicated by elevated phosphorylated MLKL (p‑MLKL) levels and severe apical membrane disruption, whereas no genotype‑dependent differences were detected in the selected markers of apoptosis, pyroptosis, or ferroptosis at 24 h. ANXA2 deficiency amplified the inflammatory response, increasing neutrophil infiltration through the upregulation of C-X-C motif chemokine ligand (CXCL) 1 and CXCL2. Mechanistically, ANXA2 associated with CHMP2A, a component of the endosomal sorting complex required for transport (ESCRT)-III membrane repair complex, following IRI, promoting ESCRT-III assembly at the apical membrane to counteract necroptosis. Knocking down CHMP2A abolished the protective effect of ANXA2. The engineered KTP-LNP@ANXA2 demonstrated excellent stability, biocompatibility, and enhanced uptake by renal TECs. Pre-treatment with KTP-LNP@ANXA2 in mice effectively delivered ANXA2 to the kidneys, attenuated IRI severity, reduced necroptosis and inflammation, and diminished neutrophil recruitment.
conclusionANXA2 confers protection against renal IRI by interacting with CHMP2A to facilitate ESCRT-III-mediated inhibition of TEC necroptosis, thereby attenuating subsequent inflammation. Enhancement of renal ANXA2 levels via engineered LNPs represents a novel and promising therapeutic strategy for preventing renal IRI.
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.