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Dysfunctional High-Density Lipoprotein Cholesterol and Coronary Artery Disease: A Narrative Review.
J Pers Med
September 2024
Division of Cardiology, Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (ProMISE), University Hospital Paolo Giaccone, University of Palermo, 90127 Palermo, Italy.
High-density lipoprotein (HDL) cholesterol is traditionally viewed as protective against cardiovascular disease (CVD). However, emerging evidence reveals that dysfunctional HDL, characterized by impaired reverse cholesterol transport (RCT), reduced anti-inflammatory and antioxidant activities and increased endothelial dysfunction, which can contribute to coronary artery disease (CAD). Dysfunctional HDL, resulting from oxidative modifications of Apolipoprotein A-1 (Apo A-1) and enzyme inactivation, fails to effectively remove cholesterol from peripheral tissues and may promote inflammation and atherosclerosis.
View Article and Find Full Text PDFMacrod1 suppresses diabetic cardiomyopathy via regulating PARP1-NAD-SIRT3 pathway.
Acta Pharmacol Sin
June 2024
Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Diabetic cardiomyopathy (DCM), one of the most serious long-term consequences of diabetes, is closely associated with oxidative stress, inflammation and apoptosis in the heart. MACRO domain containing 1 (Macrod1) is an ADP-ribosylhydrolase 1 that is highly enriched in mitochondria, participating in the pathogenesis of cardiovascular diseases. In this study, we investigated the role of Macrod1 in DCM.
View Article and Find Full Text PDFEffects of niacin and omega-3 fatty acids on HDL-apolipoprotein A-I exchange in subjects with metabolic syndrome.
PLoS One
February 2024
Cardiovascular Research Center, Sanford Research, University of South Dakota, Sioux Falls, South Dakota, United States of America.
Article Synopsis
- This study examines how niacin and omega-3 fatty acids affect HDL-apolipoprotein A-I exchange (HAE), a function of HDL related to cholesterol transport, in individuals with metabolic syndrome.
- Over 16 weeks, participants received placebo, niacin (2g/day), omega-3 (4g/day), or a combination, with results showing significant increases in HAE for both niacin (15.1%) and omega-3 (11.1%) compared to placebo.
- Notably, omega-3 therapy showed increased HAE without raising traditional markers like HDL cholesterol or apoA-I levels, indicating the assay's ability to detect functional HDL changes independent of conventional measures.
Evaluating the adverse effects and mechanisms of nanomaterial exposure on longevity of C. elegans: A literature meta-analysis and bioinformatics analysis of multi-transcriptome data.
Environ Res
April 2024
College of Textile and Clothing Engineering, Soochow University, 199 Ren-Ai Road, Suzhou, 215123, China. Electronic address:
Exposure to large-size particulate air pollution (PM2.5 or PM10) has been reported to increase risks of aging-related diseases and human death, indicating the potential pro-aging effects of airborne nanomaterials with ultra-fine particle size (which have been widely applied in various fields). However, this hypothesis remains inconclusive.
View Article and Find Full Text PDFNicotinic acid modulates microglial TREM-2 gene in Phytohaemagglutinin-Induced in vitro model of Alzheimer's disease like pathology.
Brain Res
February 2024
Dr. Panjwani Center for Molecular Medicine and Drug Research, International Center for Chemical and Biological Sciences, University of Karachi, Karachi 75270, Pakistan; H.E.J. Research Institute of Chemistry, International Center for Chemical and Biological Sciences, University of Karachi, Karachi 75270, Pakistan. Electronic address:
Alzheimer's disease (AD) is a multifactorial,neurodegenerative disorder linked withextracellular amyloid beta (Aβ) plaques deposition and formation of intracellular neurofibrillary tangles (NFTs). Currently, no effective therapies are available to cure AD. Neuroinflammation isa well-known hallmark in the onset and advancement of AD and triggering receptor expressed on myeloid cells-2 (TREM-2), a microglial gene, is responsible for regulating inflammatory responses and clearance of cellular debris.
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