Miguel Alejandro Lopez‐Ramirez

This paper identifies metformin as a potential drug for long-term treatment of cerebral cavernous malformations using AI, high-throughput screening, and animal models.

This study shows APC activates PAR1 through βarr2 and c-Src to phosphorylate Cav1 and alter its interactions with PAR1 and GRK5 in endothelial cells.

This paper identifies JUNB as a key driver of chronic brain vascular inflammation in CCM disease through multi-omic analysis of endothelial cell activation.

This study shows that silencing KRIT1 in endothelial cells under disturbed flow restores KLF2 and KLF4 expression, mimicking the transcriptomic profile of cells under laminar flow.

The paper shows that genetic inactivation of the beta1 adrenergic receptor reduces cerebral cavernous malformations in zebrafish, supporting propranolol's therapeutic effect through beta1 receptor antagonism.

This study shows that CCM lesions in mice cause behavioral impairments linked to neuroinflammation, affecting motor coordination and memory.

This study identifies neuroinflammatory astrocytes and CCM endothelium interactions that drive leukocyte recruitment and immunothrombosis in cerebral cavernous malformations, while showing that targeting endothelial NF-kB may have harmful effects.

The paper shows that astrocytes contribute to cerebral cavernous malformations (CCMs) through VEGF production driven by endothelial NO, highlighting non-cell-autonomous mechanisms.