ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2026
MLK3 promotes atherosclerosis by regulating ferroptosis in macrophages.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 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
Abstract
backgroundAtherosclerosis (AS) is the leading cause of cardiovascular death worldwide. Macrophage ferroptosis is implicated in AS progression. The precise mechanism by which mixed lineage kinase 3 (MAP3K11, MLK3) regulates macrophage ferroptosis in atherosclerosis is poorly understood.
methodsFrom the Gene Expression Omnibus (GEO) database, bulk and single-cell RNA-sequencing (scRNA-seq) datasets from vascular tissues were obtained. MLK3 was discovered to be a crucial ferroptosis-related gene (FRG) implicated in AS by means of differential analysis, weighted gene co-expression network analysis (WGCNA), and a ferroptosis gene set. Macrophages were shown to be the main cell type that expressed MLK3 when immune-infiltration profiling and single-cell RNA sequencing were combined. In vitro, macrophages were treated with Oxidized low-density lipoprotein (ox-LDL) or erastin, with or without MLK3 knockdown. Animal models assessed AS progression, ferroptosis, collagen deposition, and JNK/p53 activation. Immunofluorescence and clinical plasma MLK3 assays were performed.
resultsMLK3 was predominantly expressed in plaque macrophages. Ox-LDL upregulated MLK3 and induced ferroptosis, while MLK3 knockdown attenuated ox-LDL-induced ferroptosis by suppressing JNK/p53 signaling, without affecting erastin-induced ferroptosis. Animal models showed increased MLK3 expression, ferroptosis, JNK/p53 activation, plaque area, and collagen deposition during AS progression. Immunofluorescence confirmed MLK3 co-localization with ferroptosis-associated proteins in plaque macrophages. Plasma MLK3 levels were consistently elevated in AS patients.
conclusionMLK3 accelerates the development of atherosclerotic lesions by driving macrophage ferroptosis through JNK/p53 signaling.
Indexed as
Identifiers
42323431What 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.