IGF2BP3 stabilizes SESN1 mRNA to mitigate oxidized low-density lipoprotein-induced oxidative stress and endothelial dysfunction in human umbilical vein endothelial cells by activating Nrf2 signaling.

Atherosclerosis (AS) represents a prevalent initiating factor for cardiovascular events. Insulin-like growth factor 2 mRNA binding protein 3 (IGF2BP3) is an oncofetal RNA-binding protein that participates in cardiovascular diseases. This work aimed to elaborate the effects of IGF2BP3 on AS and the probable mechanism by using an oxidized low-density lipoprotein (ox-LDL)-induced human umbilical vein endothelial cells (HUVECs) model.

Orientin alleviates ox-LDL-induced oxidative stress, inflammation and apoptosis in human vascular endothelial cells by regulating Sestrin 1 (SESN1)-mediated autophagy.

Endothelial cells are a crucial component of the vessel-tissue wall and exert an important role in atherosclerosis (AS). To explore the role of Orientin in AS, human vascular endothelial cells (HUVECs) were induced by oxidized low-density lipoprotein (ox-LDL) to simulate the vascular endothelial injury during AS. Cell viability was detected by CCK-8 assay.

Regulation of endothelial ferroptosis by SESN1 in atherosclerosis and its related mechanism.

Background: Atherosclerosis (AS) is a disease characterized by the disorder of lipid metabolism and the formation of atherosclerotic plaques in the arterial wall, leading to arterial stenosis. Sestrins 1 (SESN1) plays an important regulatory role in AS, but the specific regulatory mechanism is still unclear.

Methods: ApoE-/- mouse models of AS were constructed.

Suppression of lncRNA attenuates myocardial infarction via / /ferroptosis axis.

Myocardial infarction (MI) is the leading cause of sudden death. Long non-doing RNAs (lncRNAs) were demonstrated to play crucial roles in multiple diseases, including cancer and cardiovascular diseases. Nevertheless, the molecular mechanism of lncNRAs in MI is unclear.

Mitochondrial targeted astaxanthin liposomes for myocardial ischemia-reperfusion injury based on oxidative stress.

Myocardial ischemia-reperfusion injury (MI/RI) refers to the clinical state of decreased coronary blood flow caused by various causes. The main pathogenesis of MI/RI is mitochondrial oxidative damage. In this study, we designed a novel mitochondrial targeted astaxanthin (AST) liposome, namely, STPP-AST-LIP, targeting mitochondria of H9c2 myocardial cells.

SESN1 attenuates the Ox‑LDL‑induced inflammation, apoptosis and endothelial‑mesenchymal transition of human umbilical vein endothelial cells by regulating AMPK/SIRT1/LOX1 signaling.

Endothelial cells are an important component of the heart and vasculature and form a crucial link between the cardiovascular system and the immune system. Sestrin 1 (SESN1) has an important role in atherosclerosis by inhibiting NOD‑like receptor family pyrin domain containing 3 inflammasome activation. However, whether SESN1 is involved in human umbilical vein endothelial cell (HUVEC) injury caused by atherosclerosis has remained to be elucidated.

Forkhead box protein 1 transcriptionally activates sestrin1 to alleviate oxidized low-density lipoprotein-induced inflammation and lipid accumulation in macrophages.

Transcription factor forkhead box protein 1 (FOXP1) has been shown cardiovascular protection. We aimed to analyze the role of FOXP1 in oxidized low-density lipoprotein (ox-LDL)-induced macrophages and its possible regulatory effect on sestrin1 (SESN1) expression. After stimulation with ox-LDL, FOXP1 expression in RAW264.