ArticleCell biology and toxicology2026
NFE2L2 suppresses microglia-mediated neuroinflammation to preserve neuronal dendritic architecture from cadmium-induced damage.
Article in Cell biology and toxicology, 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
Cadmium (Cd), a widespread environmental toxic metal, is linked to central nervous system dysfunction and neuronal structural damage, yet its mechanisms remain unclear. This study combined network toxicology with experimental validation to explore how Cd impairs dendritic integrity through neuroinflammatory pathways. Network analysis suggested that Cd-induced dendritic injury was likely mediated by inflammatory signaling pathways, with nuclear factor-erythroid 2-related factor 2 (Nfe2l2), a major redox regulator, highlighted as a candidate regulator. Therefore, we investigated the involvement of microglia-mediated neuroinflammation in Cd-induced dendritic damage and assessed the role of Nfe2l2 in this process, using Nfe2l2 knockout mice and Nfe2l2 knockdown BV2 microglia. Furthermore, primary neurons were co-cultured with conditioned media (CM) from Cd-treated microglia to evaluate how Nfe2l2-regulated neuroinflammation contributes to dendritic damage. Nfe2l2 deficiency aggravated Cd-induced dendritic damage in the hippocampus, manifested as significant reductions in dendritic length, intersections, and branch points. In parallel, Nfe2l2 deficiency also intensified Cd-induced microglial activation and neuroinflammation in the hippocampus. Consistently, Nfe2l2 knockdown amplified Cd-induced BV2 microglial activation, characterized by increased migratory and phagocytic activity, and the subsequent cytokine release. Subsequently, CM derived from these activated microglia further exacerbated neuronal dendritic damage. Moreover, Nfe2l2 knockdown diminished minocycline's anti-inflammatory and neuroprotective effects. These results demonstrate that Cd-induced microglial activation and inflammation are central to dendritic injury, and that Nfe2l2 is essential in protecting neurons from Cd-driven neuroinflammation.
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.