ArticlePloS one2025
Inhibition of PHB1/PHB2 suppresses atherosclerotic plaque formation by interrupting PI3K/AKT/mTOR signaling.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- PHB2 ameliorates ferroptosis and aortic aneurysm/dissection through NEDD4L-dependent ubiquitination of NCOA4.Redox biology · 2026Article
- CD8FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Adrenomedullin production by adult cardiac fibroblasts via NF-κB/STAT6 signaling enhances post-infarction lymphangiogenesis and cardiac repair.Scientific reports · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prohibitin 1 (PHB1) and prohibitin 2 (PHB2) are highly conserved proteins belonging to the stomatin-prohibitin flotillin-HflC/K (SPFH) protein superfamily. They are ubiquitously expressed and implicated in the regulation of cell proliferation, migration, and survival. However, the expression and biological functions of PHB1/PHB2 in atherosclerosis (AS) remain unclear. In the present study, an enzyme-linked immunosorbent assay was used to detect PHB1/PHB2 expression in the serum of patients with hyperlipidemia. The potential effect and mechanism of PHB1/PHB2 in apolipoprotein E-deficient (ApoE-/-) mice were also investigated. shRNA-PHB1 and shRNA-PHB2 lentiviruses were engineered and tail vein-injected into ApoE-/- mice fed a high-fat diet. IL-8, a proatherogenic cytokine, was used as an inducer in vitro. The effects of a PHB1/PHB2 knockdown on vascular smooth muscle cell (VSMC) proliferation, migration, and autophagy and endothelial cell (EC) adhesion were evaluated using methyl thiazolyl tetrazolium (MTT), Transwell migration, Boyden chamber, and monocyte adhesion assays, as well as transmission electron microscopy. Compared with the healthy subjects, PHB1/PHB2 expression was elevated in the serum of patients with hyperlipidemia. Animal experiments showed that downregulation of PHBs reduced the area of atherosclerotic lesions, and the expression of cyclinD1, MMP9, and LC3. In addition, in vitro experiments showed that downregulating PHB1/PHB2 expression under inflammatory stimulation reduced the adhesion, proliferation, migration, and autophagy of ECs and VSMCs by inhibiting the PI3K/Akt/mTOR pathway activation. Collectively, our findings showed that PHBs are activly associated with AS progression.
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.