Victor Collado-Diaz

TL;DR: The present review aims to shed light on this complex subject by summarizing and critically evaluating all the available clinical data regarding a relationship between ABC and cardiovascular disease, and to put forward potential pharmacological explanations compatible with both the clinical scenario and experimental findings.

TL;DR: It is found that extracellular vesicles derived from melanoma cells are rapidly transported by lymphatic vessels to draining LNs, where they selectively interact with lymphatic endothelial cells (LECs) as well as medullary sinus macrophages, suggesting that EV uptake or effector mechanisms in LECs might represent a new target for melanoma therapy.

TL;DR: The idea that biological anti-inflammatory drugs, in particular anti-TNF-α, have the capacity to influence cardiovascular risk accompanying psoriasis and rheumatoid arthritis by ameliorating vascular inflammation is endorsed.

TL;DR: In this paper, the degradation of the basement membrane surrounding lymphatic collectors and preferential up-regulation of the DC trafficking molecule VCAM-1 in collectors were identified as a critical mechanism enabling rapid dendritic cell migration to dLNs in inflammation.

TL;DR: Results showed that ABC promoted the adherence of platelets to endothelial cells, a crucial step for the formation of thrombi, which highlights the endothelium as the main cell target of ABC in this interaction, in line with previous experimental evidence that ABC induces manifestations of vascular inflammation.