Statin treatment reduces the risk of cardiovascular mortality in the general population, but it has little or no benefit in hemodialyzed (HD) patients. This may reflect different underlying pathophysiology of cardiovascular disease (CVD) in patients treated with HD, maybe involving the oxidative stress. Our aim was to assess the association of oxidized low-density lipoprotein (oxLDL), determined by Mercodia oxLDL enzyme-linked immunosorbent assay (ELISA) kit, with major adverse cardiac events (MACE) and all-cause mortality in HD patients based on the AURORA trial (rosuvastatin vs placebo), and patients not on HD from the Ludwigshafen Risk and Cardiovascular Health (LURIC) study. We also assessed whether its decrease due to statin use improves these outcomes using Cox proportional hazard models. Baseline oxLDL level was 34.2 ± 13.8 U/L in AURORA and did not differ between treatment groups, and 74.6 ± 28.1 U/L in LURIC. Lower baseline oxLDL levels were associated with higher hazard ratios (HRs) for outcomes, but not anymore after adjusting for apolipoprotein B level in AURORA and was not related to mortality in LURIC. OxLDL levels decreased by 30.9% between baseline and 3 months in the statin-treated group and increased by 10.5% between 3 and 12 months. Nevertheless, oxLDL reduction was not significantly associated with adjusted HRs for MACE and for all-cause mortality. These results showed no association between oxLDL and MACE after adjustment on apolipoprotein B, which may relate to the properties of the method used for oxLDL. Our results also showed no benefit for oxLDL reduction by rosuvastatin on outcomes. Future clinical trials are needed to define the relative CVD risks and benefits of other modalities of oxidative stress modification in this population.

Download full-text PDF

Source
http://dx.doi.org/10.1080/10715762.2016.1241878DOI Listing

Publication Analysis

Top Keywords

oxldl
9
mortality patients
8
risk cardiovascular
8
oxidative stress
8
mace all-cause
8
all-cause mortality
8
baseline oxldl
8
oxldl levels
8
oxldl reduction
8
mortality
5

Similar Publications

The study was designed to investigate the impact of N6-methyladenosine (m6A) writer Wilms tumor 1-associated protein (WTAP) on the progression of atherosclerosis (AS) and to further elucidate its possible regulatory mechanism. The m6A levels and WTAP expressions were initially assessed through RIP, qRT-PCR, and western blotting. An in vitro model of AS was constructed by ox-LDL treatment in RAW264.

View Article and Find Full Text PDF

PIM1 instigates endothelial-to-mesenchymal transition to aggravate atherosclerosis.

Theranostics

January 2025

Department of Neurosurgery, Qilu Hospital, Cheeloo College of Medicine and Institute of Brain and Brain-Inspired Science, Shandong University, Shandong, China.

Endothelial-to-mesenchymal transition (EndMT) is a cellular reprogramming mechanism by which endothelial cells acquire a mesenchymal phenotype. Endothelial cell dysfunction is the initiating factor of atherosclerosis (AS). Increasing evidence suggests that EndMT contributes to the occurrence and progression of atherosclerotic lesions and plaque instability.

View Article and Find Full Text PDF

CD36-mediated uptake of oxidized LDL induces double-negative regulatory T cell ferroptosis in metabolic dysfunction-associated steatotic liver disease.

Metabolism

December 2024

Medical Research Center, Beijing Institute of Respiratory Medicine and Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China; Department of Gastroenterology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China; Immunology Research Center for Oral and Systemic Health, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China. Electronic address:

Background: Metabolic alterations have been shown to instigate liver inflammation in metabolic dysfunction-associated steatotic liver disease (MASLD), but the underlying mechanism is not fully elucidated. During MASLD progression, intrahepatic CD3TCRαβCD4CD8 double negative T regulatory cells (DNT) decrease cell survival and immunosuppressive function, leading to aggravated liver inflammation. In this study, we aim to reveal the underlying mechanisms that cause changes in DNT during MASLD progression.

View Article and Find Full Text PDF

Given the heightened risk of diabetes-related cardiovascular events associated with inactivity, this study investigates the molecular mechanisms of vascular damage in streptozotocin (STZ)-induced diabetic rats. The aim is to elucidate the impact of different exercises (interval and continuous training) and metformin on biochemical parameters, aortic injury, oxidative stress, and inflammation to provide insights into potential therapeutic interventions for diabetes-associated vascular complications. Male Wistar rats were administered a single dose of STZ (60 mg/kg) to induce diabetes.

View Article and Find Full Text PDF

This study is aimed at investigating the effects of atorvastatin (ATV) on endothelial cell injury in atherosclerosis (AS) through inhibiting acyl-CoA synthetase long-chain family member 4 (ACSL4)-mediated ferroptosis. Human umbilical vein endothelial cells (HUVECs) were treated with oxidized low-density lipoprotein (ox-LDL) to establish an in vitro model of AS. The cell viability, lactate dehydrogenase (LDH) release, apoptosis, and expression levels of apoptotic proteins were assessed.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!