2-Acetamidophenol (2-AAP) Suppresses the Progression of Atherosclerosis by Alleviating Hyperlipidemia and Attenuating the Ferroptosis Pathway DOI Creative Commons

Xiaohan Zang,

Yongcheng Wang, Cong Han

et al.

Marine Drugs, Journal Year: 2024, Volume and Issue: 22(11), P. 513 - 513

Published: Nov. 13, 2024

Hyperlipidemia and consequent endothelial inflammation, along with foam cell generation, promote the progression of atherosclerosis (AS). Here, we aimed to investigate effects 2-acetamidophenol (2-AAP), which was selected by zebrafish phenotypic screening, in alleviating AS relieving hyperlipidemia inhibiting formation, as well underlying mechanisms. In a model, 2-AAP increased lipid-lowering efficacy; alleviated TC, TG, LDL-C, MDA levels; elevated HDL-C T-SOD significantly improved intravascular macrophage aggregation; blood flow. an ox-LDL-induced RAW264.7 inhibited lipid phagocytosis cells; reduced intracellular FC, CE contents; decreased CE/TC ratio, thus slowing generation. addition, ROS ferrous ion accumulation cells, content, GPX4 viability. Furthermore, transcriptome analyses gene expression validation showed treatment upregulates genes related GSH synthesis transport, such gclc, gclm, gss, gpx4a, enhanced levels involved storage transportation iron ions, fpn1, fth, g6pd, indicating that dramatically regulated ferroptosis glutathione metabolic pathways. Overall, our study demonstrated potential attenuating pathway provided evidence supporting future application treatment.

Language: Английский

Cellular Phenotypic Transformation During Atherosclerosis: The Potential Role of miRNAs as Biomarkers DOI Open Access

Souhir Wassaifi,

Bertrand Kaeffer, Sinda Zarrouk‐Mahjoub

et al.

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(5), P. 2083 - 2083

Published: Feb. 27, 2025

Cellular phenotypic transformation is a key process that occurs during the development and progression of atherosclerosis. Within arterial wall, endothelial cells, vascular smooth muscle macrophages undergo changes contribute to pathogenesis miRNAs have emerged as potential biomarkers for cellular Monitoring miR-155-5p, miR-210-3p, miR-126-3p or 5p levels could provide valuable insights into disease progression, risk complications, response therapeutic interventions. Moreover, miR-92a-3p's elevated in atherosclerotic plaques present opportunities predicting related complications. Baseline miR-33a/b hold responses cholesterol-lowering therapies, such statins, likelihood dyslipidemia-related Additionally, assessment miR-122-5p may offer efficacy low-density-lipoprotein-lowering therapies. Understanding specific miRNA-mediated regulatory mechanisms involved transformations can atherosclerosis potentially identify novel targets.

Language: Английский

Citations

0
MicroRNA Inhibiting Atheroprotective Proteins in Patients with Unstable Angina Comparing to Chronic Coronary Syndrome DOI Open Access
Michał Kowara, Michał Kopka,

Karolina Kopka

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(19), P. 10621 - 10621

Published: Oct. 2, 2024

Patients with unstable angina present clinical characteristics of atherosclerotic plaque vulnerability, contrary to chronic coronary syndrome patients. The process athersclerotic destabilization is also regulated by microRNA particles. In this study, the investigation on expression levels microRNAs inhibiting proteins that protect from progression (miR-92a KLF2, miR-10b KLF4, miR-126 MerTK, miR-98 IL-10, miR-29b TGFβ1) was undertaken. A number 62 individuals were enrolled—unstable (UA, n = 14), (CCS, 38), and healthy volunteers (HV, 10). Plasma samples taken, assessed qRT-PCR. As a result, UA patients presented significantly increased compared CCS (0.097 vs. 0.058, p 0.033). Moreover, in additional analysis when grouped together stable significant left main or proximal anterior descending (“UA LM/proxLAD” group, 29 patients) lesions other regions circulation (“CCS other” 25 both (0.104 0.046; 0.0032) miR-92a (92.64 54.74; 0.0129) elevated. conclusion, study revealed miR-92a, regulator endothelial protective KLF factors (KLF4 respectively) more vulnerable phenotypes.

Language: Английский

Citations

0
Omics research in atherosclerosis DOI

Kai-Jiang Tian,

Yang Yu,

G. Chen

et al.

Molecular and Cellular Biochemistry, Journal Year: 2024, Volume and Issue: unknown

Published: Oct. 24, 2024

Language: Английский

Citations

0
2-Acetamidophenol (2-AAP) Suppresses the Progression of Atherosclerosis by Alleviating Hyperlipidemia and Attenuating the Ferroptosis Pathway DOI Creative Commons

Xiaohan Zang,

Yongcheng Wang, Cong Han

et al.

Marine Drugs, Journal Year: 2024, Volume and Issue: 22(11), P. 513 - 513

Published: Nov. 13, 2024

Hyperlipidemia and consequent endothelial inflammation, along with foam cell generation, promote the progression of atherosclerosis (AS). Here, we aimed to investigate effects 2-acetamidophenol (2-AAP), which was selected by zebrafish phenotypic screening, in alleviating AS relieving hyperlipidemia inhibiting formation, as well underlying mechanisms. In a model, 2-AAP increased lipid-lowering efficacy; alleviated TC, TG, LDL-C, MDA levels; elevated HDL-C T-SOD significantly improved intravascular macrophage aggregation; blood flow. an ox-LDL-induced RAW264.7 inhibited lipid phagocytosis cells; reduced intracellular FC, CE contents; decreased CE/TC ratio, thus slowing generation. addition, ROS ferrous ion accumulation cells, content, GPX4 viability. Furthermore, transcriptome analyses gene expression validation showed treatment upregulates genes related GSH synthesis transport, such gclc, gclm, gss, gpx4a, enhanced levels involved storage transportation iron ions, fpn1, fth, g6pd, indicating that dramatically regulated ferroptosis glutathione metabolic pathways. Overall, our study demonstrated potential attenuating pathway provided evidence supporting future application treatment.

Language: Английский

Citations

0