PhD student Sichuan University Chengdu, Sichuan, China (People's Republic)
Introduction: Pulmonary arterial smooth muscle cells (PASMCs) display a hyperproliferative, apoptosis-resistant phenotype, which is promoted by endoplasmic reticulum (ER) stress and mitochondrial calcium uniporter (MCU) dysfunction, is a key driver of the vessel remodeling in pulmonary arterial hypertension (PAH)[1, 2]. Inducing PASMCs apoptosis through synergistic modulation of the ER-mitochondria to reverse vascular remodeling would be an effective therapeutic strategy for PAH. However, the precise therapeutics delivery to pulmonary artery presents a significant challenge due to the persistent hemodynamic shear stress and relatively high blood flow velocity，let alone to ER of PASMCs.
Learning Objectives:
Understand a novel biomimetic ER-targeted delivery system.
Understand a strategy to reverse occlusive vessel remodeling of PAH by attenuating ER stress and regulating MCU.
