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Abstract
RBMS1 deficiency in a mouse model is associated with increased thrombus formation and impaired endothelial cell function.
- RNA-binding proteins, particularly RBMS1, may play a significant role in the development of deep vein thrombosis (DVT).
- In mice lacking RBMS1 specifically in endothelial cells, thrombus formation is exacerbated.
- RBMS1 is linked to the stability of autophagy-related 3 (ATG3) mRNA, which is crucial for maintaining autophagy in vascular endothelial cells.
- Loss of RBMS1 leads to destabilization of ATG3 mRNA, resulting in reduced autophagic activity and compromised endothelial integrity.
- Overexpression of ATG3 can counteract the negative effects of RBMS1 depletion, suggesting a potential pathway for therapeutic intervention.
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