Endothelial dysfunction of syphilis: Pathogenesis

Abstract

Treponema pallidum is the causative factor of syphilis, a sexually transmitted disease (STD) characterized by perivascular infiltration of inflammatory cells, vascular leakage, swelling and proliferation of endothelial cells (ECs). The endothelium lining blood and lymphatic vessels is a key barrier separating body fluids from host tissues and is a major target of T. pallidum. In this review, we focus on how T. pallidum establish intimate interactions with ECs, triggering endothelial dysfunction such as endothelial inflammation, abnormal repairment and damage of ECs. In addition, we summarize that migration and invasion of T. pallidum across vascular ECs may occur through two pathways. These two mechanisms of transendothelial migration are paracellular and cholesterol‐dependent, respectively. Herein, clarifying the relationship between T. pallidum and endothelial dysfunction is of great significance to provide novel strategies for diagnosis and prevention of syphilis, and has a great potential prospect of clinical application.

Kaempferol Rescues Vascular Endothelial Ferroptosis by Inhibiting Lipid Peroxidation

“…They are pivotal in promoting multi-organ health and homeostasis through the regulation of solute permeability, shear stress response, vasodilatory tone maintenance, and their ability to exhibit both anti-inflammatory and pro-inflammatory, as well as antioxidant and prooxidant activities 3,4 . Evidence increasingly supports the involvement of endothelial cell death in the onset and progression of vascular diseases [5][6][7] . Cell death, an evolutionary conserved process, serves to regulate cell populations by eliminating excessive, damaged, or senescent cells 8 .…”