Proliferation, migration and phenotypic transformation of VSMC induced via Hcy related to up-expression of WWP2 and p-STAT3.
Level 5 - mechanism / opinion, no new human data
Preclinical animal model (ApoE-/- mice) and in vitro laboratory study without human data.
PubMed 38166045 · doi:10.1371/journal.pone.0296359
What was done
In vitro vascular smooth muscle cell assays and ApoE-deficient mouse models of hyperhomocysteinemia were used to investigate the mechanisms by which homocysteine influences cell proliferation, migration, and phenotypic transformation, specifically evaluating the involvement of WWP2, SIRT1/STAT3, and the UTX/H3K27me3 axis.
What was found
The abstract reports no numerical data, sample sizes, or effect sizes. Directionally, homocysteine upregulated WWP2 expression through UTX-dependent inhibition of histone H3K27me3, and WWP2 subsequently promoted vascular smooth muscle cell proliferation, migration, and phenotype switching by increasing SIRT1/STAT3 phosphorylation.
Why it matters
This study delineates a specific molecular pathway linking elevated homocysteine to vascular smooth muscle cell dysfunction, presenting WWP2 as a potential preclinical target in atherosclerosis research.
Limits
The study is entirely preclinical, relying on rodent models and cell culture without human clinical data. The abstract provides no quantitative metrics, exact sample sizes, or statistical confidence intervals.
Cited by
- supports Homocysteine drives cardiovascular smooth muscle proliferation and leads to heart attacks.