PACS2 initiates foam cell formation in macrophages through the ROS-PPARγ-CD36 positive feedback loop.

Disrupted mitochondria-associated endoplasmic reticulum membrane (MAM) homeostasis is closely linked to obesity-related diseases and insulin resistance pathogenesis. The formation of foam cells with classically activated lipid uptake by macrophages is an important mechanism in the progression of atherosclerosis. This study investigated the effects of the MAM interface anchor protein, phosphofurin acidic cluster sorting protein 2 (PACS2), on atherosclerosis.

S1PR2 Mediates Smooth Muscle Cell Proliferation and Endothelial Cell Permeability via Akt/mTOR and RhoA/ROCK1 in Atherosclerosis.

Atherosclerosis is a complex disease involving a series of interrelated events, among which endothelial cell dysfunction and vascular smooth muscle cell proliferation play pivotal roles in the early formation of atherosclerotic plaques. Sphingosine 1-phosphate, a product of sphingomyelin metabolism, serves as a signaling molecule implicated in the pathogenesis of atherosclerosis and other conditions by binding to sphingosine 1-phosphate receptors (S1PRs). However, the precise mechanism by which S1PRs influence atherosclerosis remains incompletely understood.

miR-145 Alleviates Smooth Muscle Cell Phenotype Transition via ADAM17-Mediated ACE2 Shedding.

It has been shown that miR-145 is involved in the differentiation of vascular smooth muscle cells (VSMCs) and may regulate vascular remodeling. However, the molecular mechanisms behind these pathological processes in hypertension are not fully elucidated. The present study was to examine whether miR-145 modulates phenotypic transformation of VSMCs under normal state and synthetic state and to explore the possible role of ADAM17-mediated ACE2 shedding and ACE2-Ang-(1-7)-Mas receptor axis.

The Role of ADAM17 in Inflammation-Related Atherosclerosis.

Atherosclerosis is a chronic inflammatory disease that poses a huge economic burden due to its extremely poor prognosis. Therefore, it is necessary to explore potential mechanisms to improve the prevention and treatment of atherosclerosis. A disintegrin and metalloprotease 17 (ADAM17) is a cell membrane-bound protein that performs a range of functions through membrane protein shedding and intracellular signaling.