Alma Zernecke

TL;DR: It is shown that endothelial cell–derived apoptotic bodies are generated during atherosclerosis and convey paracrine alarm signals to recipient vascular cells that trigger the production of CXCL12.

TL;DR: Targeting MIF in individuals with manifest atherosclerosis can potentially be used to treat this condition and displays chemokine-like functions and acts as a major regulator of inflammatory cell recruitment and atherogenesis.

TL;DR: The surprising contribution of granulocyte subsets and mast cells to early atherogenesis and subsequent plaque instability is highlighted, and the complex, double-edged role of monocyte, macrophage and dendritic-cell subsets through crosstalk with T cells and vascular progenitor cells is described.

TL;DR: It is shown that enforced survival of monocytes and plaque-resident phagocytes, including foam cells, restored atherogenesis in CX(3)CR1-deficent mice and introduced a Bcl2 transgene, suggesting that the CX (3)C axis provides an essential survival signal.

TL;DR: Stable peptide inhibitors are designed that specifically disrupt proinflammatory CCL5-CXCL4 interactions, thereby attenuating monocyte recruitment and reducing atherosclerosis without the aforementioned side effects.