AI Article Synopsis
- - Angiogenesis is the process of forming new blood vessels, which is vital for organ development, but how it's controlled at the genetic level is not fully understood.
- - Research shows that the gene FOXC1 is crucial for the growth of blood vessels in the retina; its loss affects certain amino acid transporters and reduces activity of the mTOR pathway, which is important for cell growth.
- - FOXC1 is necessary not only for retinal blood vessel formation but also for the function of pericytes, essential for the blood-retina barrier, highlighting its potential as a target for therapies aimed at retinal vascular diseases.
Article Abstract
Angiogenesis, the growth of new blood vessels from pre-existing vasculature, is essential for the development of new organ systems, but transcriptional control of angiogenesis remains incompletely understood. Here we show that FOXC1 is essential for retinal angiogenesis. Endothelial cell (EC)-specific loss of Foxc1 impairs retinal vascular growth and expression of Slc3a2 and Slc7a5, which encode the heterodimeric CD98 (LAT1/4F2hc) amino acid transporter and regulate the intracellular transport of essential amino acids and activation of the mammalian target of rapamycin (mTOR). EC-Foxc1 deficiency diminishes mTOR activity, while administration of the mTOR agonist MHY-1485 rescues perturbed retinal angiogenesis. EC-Foxc1 expression is required for retinal revascularization and resolution of neovascular tufts in a model of oxygen-induced retinopathy. Foxc1 is also indispensable for pericytes, a critical component of the blood-retina barrier during retinal angiogenesis. Our findings establish FOXC1 as a crucial regulator of retinal vessels and identify therapeutic targets for treating retinal vascular disease.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11099035 | PMC |
| http://dx.doi.org/10.1038/s41467-024-48134-2 | DOI Listing |
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