Atherosclerosis remains the underlying process responsible for cardiovascular diseases and the high mortality rates associated. This chronic inflammatory disease progresses with the formation of occlusive atherosclerotic plaques over the inner walls of vascular vessels, with oxidative stress being an important element of this pathology. Oxidation of low-density lipoproteins (ox-LDL) induces endothelial dysfunction, foam cell activation, and inflammatory response, resulting in the formation of fatty streaks in the atherosclerotic wall. With this in mind, different approaches aim to reduce oxidative damage as a strategy to tackle the progression of atherosclerosis. Special attention has been paid in recent years to the transcription factor Nrf2 and its downstream-regulated protein heme oxygenase-1 (HO-1), both known to provide protection against atherosclerotic injury. In the current review, we summarize the involvement of oxidative stress in atherosclerosis, focusing on the role that these antioxidant molecules exert, as well as the potential therapeutic strategies applied to enhance their antioxidant and antiatherogenic properties.
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http://dx.doi.org/10.3390/antiox10091463 | DOI Listing |
Tissue Cell
January 2025
Department of Human and Animal Physiology, Yerevan State University, Yerevan, 1 Alek Manukyan St, Yerevan 0025, Armenia; Research Institute of Biology, Yerevan State University, Yerevan, 1 Alek Manukyan St, Yerevan 0025, Armenia. Electronic address:
High altitude characterized by the low partial pressure of the oxygen is a life-threatening condition that contributes to the development of acute pulmonary edema and hypoxic lung injury. In this study, we aimed to investigate the contribution of some inflammatory and oxidative stress markers along with antioxidant system enzymes in the pathogenesis of HAPE (high-altitude pulmonary edema) formation. We incorporated the study on 42 male rats to unravel the role of mast cells (MCs) and TNF-α in the lung after the effect of acute hypobaric hypoxia.
View Article and Find Full Text PDFJ Bras Pneumol
January 2025
. Departamento de Biologia Geral, Universidade Federal Fluminense, Niterói (RJ) Brasil.
Objective: Silicosis is a pneumoconiosis characterized by fibrosis of the lung parenchyma caused by the inhalation of silica particles. Silica dust inhalation is associated with inflammation and induction of oxidative stress in the lungs. This oxidative stress affects telomeres, which are short tandem DNA repeats that cap the end of linear chromosomes.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Immunobiology, Institute of Biological Sciences, Faculty of Biology and Biotechnology, Maria Curie-Skłodowska University, Lublin, Poland.
The aim of this study was to investigate the changes in the level of oxidative stress and lysozyme-like and phenoloxidase (PO) activity under the influence of nosemosis. Honeybees were kept in natural (apiary) and artificial (laboratory) conditions. In this study, it was shown for the first time that honeybees kept in apiaries have higher levels and activity of the studied parameters than honeybees kept in the laboratory.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Biological Sciences, Purdue University Fort Wayne, Fort Wayne, Indiana, United States of America.
Present study aimed at improving the immune and antioxidant response of Pacific white shrimp (Litopenaeus vannamei) cultured at high stocking density fed with 0.2% supplementation of lauric acid (LA) and N-acetyl-L-cysteine (NAC). Shrimp (initial average weight = 0.
View Article and Find Full Text PDFDiscov Oncol
January 2025
Western Institute of Digital-Intelligent Medicine, 401329, Chongqing, China.
Background: The metabolism of stearoyl-GPE plays a key role in the liver metastasis of gastric cancer. This investigation delves into the mechanisms underlying the intricate tumor microenvironment (TME) heterogeneity triggered by stearoyl metabolism in gastric cancer with liver metastasis (LMGC), offering novel perspectives for LMGC.
Objective: Utilizing Mendelian randomization, we determined that stearoyl metabolism significantly contributes to the progression of gastric cancer (GC).
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