ArticleCell biochemistry and biophysics2025
Down-regulation of ATP8B2 in Foam Cells Inhibits Autophagic Flux and ox-LDL Degradation in Atherosclerosis.
Article in Cell biochemistry and biophysics, 2025. 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
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
1 citing paper in PubMed.
- Effects of β‑hydroxybutyrate on restoring autophagic flux and mitochondrial function in macrophages exposed to oxidized low‑density lipoprotein.Molecular medicine reports · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our study aims to screen and explore the potential molecular mechanisms of atherosclerosis using a comprehensive research approach combining bioinformatics analysis and molecular biology experiments. Bioinformatics analyses were conducted to screen for key genes with significantly differential expression in atherosclerosis. Subsequently, macrophages and foam cells induced from THP-1 cells were utilized to validate the function of these key genes through siRNA knockdown. Molecular biology experiments encompassed reverse transcription polymerase chain reaction (RT-PCR), Western Blotting, immunofluorescence staining, and JC-1 probe detection of mitochondrial membrane potential. ATP8B2, encoding a P4-ATPase, was significantly downregulated in both plaque tissues and circulating macrophages of atherosclerosis patients. This enzyme influences membrane fusion and other dynamic processes by affecting the asymmetric distribution of phospholipids within the bilayer. Knockdown of ATP8B2 expression significantly inhibited autophagic flux in macrophages, manifested by abnormal accumulation of LC3-II and p62 protein levels. Furthermore, downregulation of ATP8B2 expression significantly inhibited the degradation of oxidized low-density lipoprotein (ox-LDL) by macrophages. Simultaneously, reduced ATP8B2 expression led to decreased mitochondrial membrane potential and mitochondrial dysfunction. Our study unveils for the first time the crucial role of ATP8B2 in atherosclerosis, particularly in maintaining autophagic flux, promoting ox-LDL degradation, and sustaining mitochondrial homeostasis.
Indexed as
Identifiers
40148707What 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.