Endothelial Matrin-3 deficiency, senescence and atherosclerosis in mice
In this mouse and cell study, silencing or deleting endothelial Matrin-3 was linked to endothelial senescence and, in mice, to larger atherosclerotic lesions and altered lipid levels. Matrin-3 was reduced in mouse and human plaques. [1]
Automatic summary · not editorially reviewed
The key findings
Silencing Matrin-3 in human endothelial cells in vitro induced senescence, with reduced proliferation, increased senescence-associated β-galactosidase activity and impaired mitochondrial function. [1]
In a mouse atherosclerosis model, endothelial cell-specific Matrin-3 deficiency increased atherosclerotic lesion area by 1.41-fold and was associated with higher plasma and hepatic lipids. [1]
Matrin-3 expression was reduced in mouse and human atherosclerotic plaques. [1]
The source at a glance
- Study type / format
- Preclinical laboratory study (cell-culture experiments and a mouse model), reported in an abstract.
- Population / context
- Human endothelial cells in vitro and mice (Matrin-3 floxed on a low-density lipoprotein receptor-knockout background with an endothelial cell-specific, tamoxifen-inducible Cre driver); mouse and human atherosclerotic plaques.
- Summary based on
- Study abstract
- Original publication
- October 1, 2026
Matrin-3 silencing in human endothelial cells
The authors first asked what happens when Matrin-3 is silenced in human endothelial cells in vitro. Silencing induced endothelial senescence: cell proliferation fell, senescence-associated β-galactosidase activity rose, and mitochondrial function was impaired. Protein and RNA measurements found hundreds of differentially expressed genes and proteins. Pathway analyses pointed to DNA replication, p53 signaling, cell-cycle regulation and cellular senescence. These are cell-culture observations; they do not show effects on lifespan or on human disease.
Supporting source [1]
Larger lesions in mice lacking endothelial Matrin-3
To test the role in atherosclerosis, the team bred mice with a floxed Matrin-3 gene on a low-density lipoprotein receptor-knockout background and crossed them with mice carrying an endothelial cell-specific, tamoxifen-inducible Cre driver. In this mouse atherosclerosis model, endothelial cell-specific Matrin-3 deficiency increased atherosclerotic lesion area by 1.41-fold. It was associated with higher plasma low-density lipoprotein cholesterol and triglycerides, higher hepatic cholesterol and triglycerides, and substantial transcriptional changes in the aortic intima. The deficiency also induced hepatic steatosis, fibrosis, inflammation and endothelial senescence. These are associations in mice, not proof that Matrin-3 loss causes human atherosclerosis.
Supporting source [1]
Liver reprogramming and reduced Matrin-3 in plaques
Single-nucleus RNA sequencing of the liver showed transcriptional reprogramming of hepatocytes, including changes in pathways for lipid metabolism, inflammation and constitutive androstane receptor signaling. The authors describe this as consistent with a functional link between endothelial Matrin-3 deficiency and hepatocyte transcriptional responses. Finally, Matrin-3 expression was reduced in mouse and human atherosclerotic plaques. This abstract reports an abstract-level summary only; the full text was not reviewed, so details of design, sample sizes and follow-up are not available here.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Findings come from cell-culture experiments and a mouse model, and the mouse lesion and lipid results are associations, not proof of cause in humans. Design details, sample sizes and follow-up are not reported in the abstract.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Cheng X, Tanni FY, Zoni RN, Abdollahi E, Childs E, Sun X. · europepmc.org · October 1, 2026