Ingrid Fleming

This paper identifies immunomodulatory endothelial cells (IMEC) that present antigens on MHC class II and activate T cells in atherosclerosis.

The paper identifies the transaminase-omega-amidase pathway as a redox-sensitive metabolic switch in endothelial glutamine metabolism, showing that NIT2 oxidation inhibits its activity and affects angiogenesis.

This study shows that pericyte contact promotes endothelial cell metabolism by transferring lactate via SLC16A3, altering acetylome and lactylome, and enhancing EndMT-like processes.

This study identifies SMOC1 as a regulator of EndMT in cardiac repair, showing its role in modulating TGF-β/endoglin signaling and preventing pathological fibrosis after MI.

This study shows that soluble epoxide hydrolase in astrocytes contributes to vascular instability in Alzheimer's disease, and its deletion reduces vascular amyloid burden and preserves vascular structure.

This study identifies ferroptosis as a regulator of lymphatic vessel growth and regression, showing its role in development and injury response through metabolic and lipid pathway mechanisms.

This study identifies miP-PSTPIP2, an inflammation-induced microprotein that modulates endothelial cell endocytosis, cytoskeleton dynamics, and barrier function by affecting Arp2/3-mediated actin dynamics.

This study identifies nuclear eNOS's role in modulating ADAR1 activity and type I interferon signaling, linking NO bioavailability to endothelial function and atherogenesis.

This paper designs and tests sEH-PROTACs to degrade soluble epoxide hydrolase, identifying PROTAC 23 as effective in degrading sEH in human macrophages.

This study shows that DNMT3A mutations in CHIP lead to metabolic changes in macrophages that drive inflammation, and targeting these changes can improve heart failure outcomes.

This study shows that loss of RGS5 in pericytes with age leads to cardiac dysfunction and fibrosis by altering pericyte function and activating fibroblasts.