Objectives: Psoriasis is a chronic inflammatory skin disease. Chronic inflammation results in increased oxidative stress and oxidizes lipoproteins, increasing their atherogenicity. This study sought to estimate the levels of oxidized low-density lipoprotein (ox-LDL) and antibodies against oxidized LDL (anti-ox-LDL) and compute the ratio of anti-ox-LDL/ox-LDL as a single composite parameter to assess the oxidative lipoprotein burden as an indicator of cardiovascular risk in patients with psoriasis.
Methods: This cross-sectional study included 45 patients with psoriasis. All patients were given a psoriasis severity index score and their ox-LDL and anti-ox-LDL estimated using ELISA.
Results: The results of this study show an elevation in the ratio of anti-ox-LDL to ox-LDL in patients with psoriasis, which initiate and perpetuate the pathogenesis of psoriasis and its comorbidity, atherosclerotic cardiovascular disease.
Conclusions: Our results suggest that an elevated ratio of anti-ox-LDL/ox-LDL can serve as a composite parameter reflecting the total oxidative lipoprotein burden and cardiovascular risk in psoriasis patients.
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http://dx.doi.org/10.5001/omj.2016.78 | DOI Listing |
Clin Transl Med
January 2025
Vascular Research Laboratory, IIS-Fundación Jiménez Díaz, Madrid, Spain.
Background: Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipids and leukocytes within the arterial wall. By studying the aortic transcriptome of atherosclerosis-prone apolipoprotein E (ApoE) mice, we aimed to identify novel players in the progression of atherosclerosis.
Methods: RNA-Seq analysis was performed on aortas from ApoE and wild-type mice.
Talanta
January 2025
Department of Chemistry and Center of Excellence for Innovation in Chemistry, Faculty of Science, Ubon Ratchathani University, Ubon Ratchathani, 34190, Thailand.
Oxidized low-density lipoprotein (oxLDL) is the leading cause of atherosclerosis and cardiovascular disease development. An enzyme-linked immunosorbent assay (ELISA)-mimic system for sensitive and specific oxLDL determination was developed using selective aptamer-molecularly imprinted polymer nanoparticles (AP-MIP NP) coupled with an immunology-based colorimetric assay. The AP-MIP NP were synthesized using solid-phase molecular imprinting by incorporating aptamers into the MIP NP cavities.
View Article and Find Full Text PDFCurr Mol Pharmacol
January 2025
Department of Cardiology, Second Hospital of Shanxi Medical University, Taiyuan, Shanxi Province, 030001, China.
Background And Aims: Atherosclerosis is a chronic cardiovascular disease which is regarded as one of the most common causes of death in the elderly. Recent evidence has shown that atherosclerotic patients can benefit by targeting interleukin-1 beta (IL-1β). Aloperine (ALO) is an alkaloid which is mainly isolated from L.
View Article and Find Full Text PDFZhongguo Zhong Yao Za Zhi
December 2024
School of Basic Medical Sciences, Guangzhou University of Chinese Medicine Guangzhou 511400, China.
The aim of this study was to investigate the underlying mechanism of chrysophanol(Chr) in reducing inflammation and foam cell formation induced by oxidized low-density lipoprotein(ox-LDL) and to investigate the targets and pathways related to effects of Chr on coronary atherosclerosis, providing a theoretical basis for the development of new clinical drugs. RAW264.7 macrophages were cultured in vitro, and after determining the appropriate concentrations of Chr and ox-LDL for treating RAW264.
View Article and Find Full Text PDFBiotechnol Bioeng
January 2025
Chair of Technical Biochemistry, Technische Universität Dresden, Dresden, Saxony, Germany.
Ikarugamycin is a member of the natural product family of the polycyclic tetramate macrolactams (PoTeMs). The compound exhibits a diverse range of biological activities, including antimicrobial, antiprotozoal, anti-leukemic, and anti-inflammatory properties. In addition, it interferes with several crucial cellular functions, such as oxidized low-density lipoprotein uptake in macrophages, Nef-induced CD4 cell surface downregulation, and mechanisms of endocytosis.
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