# Un-sweetening the deal: targeting glucose metabolism in brain arteriovenous malformations

## TL;DR

This paper explores how abnormal glucose metabolism in blood vessels contributes to brain arteriovenous malformations and suggests targeting this process for treatment.

## Contribution

The study reveals a novel role of KRAS-dependent glycolytic reprogramming in the development of sporadic arteriovenous malformations.

## Key findings

- KRAS-dependent glycolytic reprogramming occurs in endothelial cells of sporadic arteriovenous malformations.
- Targeting glucose metabolism may offer new therapeutic strategies for treating brain arteriovenous malformations.

## Abstract

Brain arteriovenous malformations (bAVMs) are vascular anomalies characterized by a knot of intertwined and enlarged blood vessels. They form atypical direct connections (shunts) between the arterial and venous sides of the circulation, bypassing the capillary bed. This pathological flow pattern exposes fragile veins to excess mechanical stress, predisposing them to rupture. Although the incidence of bAVMs is low, their clinical impact is substantial as rupture results in intracranial hemorrhage, which often leads to severe neurological consequences including stroke (Samaniego et al, 2024).

T. Haas and M. Rudnicki discuss the study by Wu et al, in this issue of EMBO Mol Med, that describes KRAS-dependent glycolytic reprogramming of endothelial cells in sporadic arteriovenous malformations.