Vascular diseases articles from across Nature Portfolio

Vascular protein disulfide isomerase (PDI) regulates thrombosis and targeting extracellular PDI remains a promising antithrombotic approach. Here, the authors show that PDI cleaves allosteric disulfides on histidine-rich glycoprotein to influence its functions during coagulation and thus fine-tune the kinetics of thrombus formation.

Here, the authors perform a large exome-wide study for venous thromboembolism and identify 18 potential risk genes, including 4 new genes, revealing a significant role of rare coding variants, and offering insights into genetic risk factors.

Yurdagul and colleagues offer an integrated picture of metabolic changes at the cellular and at the lesion level in atherosclerosis.

In ST-segment elevation myocardial infarction, the role of interventional modification of thrombi in the coronary arteries before stenting is controversial. However, innovations in stroke intervention have sparked renewed interest in thrombus modification approaches. We discuss current and emerging techniques to extract or disperse thrombi, aiming to reduce downstream embolization, microvascular obstruction and myocardial injury.

A new study identifies a hormone that is secreted by the gut in response to cholesterol absorption and can inhibit cholesterol synthesis in the liver, which prevents an increase in circulating cholesterol levels.

Shoaran and Maffia recount how our understanding of the role of inflammation in atherosclerosis has evolved and highlight the study by Göran Hansson and colleagues that provided the first hint of the involvement of the adaptive immune response in atherosclerosis.

Hepatocytes are recognized as having a primary role in production and clearance of apolipoprotein B100-containing lipoproteins. A new study finds that Kupffer cells can respond to the initial atherogenic dyslipidemia and regulate levels of circulating lipoprotein.

A metabolic product of excess niacin promotes vascular inflammation in preclinical models and is associated with increased rates of major adverse cardiovascular events in humans.

Anti-inflammatory therapy involving IL-1β inhibition might reduce the risk of cardiovascular events in individuals with clonal haematopoiesis by increasing the number of fibroblast-like cells in the fibrous cap region of atherosclerotic plaques, thereby stabilizing the plaque and reducing the likelihood of rupture.