Secondary dyslipidemia: its treatments and association with atherosclerosis

Global Health & Medicine, Journal Year: 2020, Volume and Issue: 3(1), P. 15 - 23

Published: Dec. 13, 2020

Dyslipidemia is classified into primary and secondary types. Primary dyslipidemia basically inherited caused by single or multiple gene mutations that result in either overproduction defective clearance of triglycerides cholesterol. Secondary unhealthy lifestyle factors acquired medical conditions, including underlying diseases applied drugs. accounts for approximately 30-40% all dyslipidemia. should be treated finding addressing its causative For example, treatment dyslipidemia, such as hyperlipidemia due to hypothyroidism, using statin without controlling may lead myopathy serious adverse events rhabdomyolysis. Differential diagnosis very important safe effective treatment. Here, we describe an overview about drugs interfere with lipid metabolism leading Further, show the association each atherosclerosis treatments

Language: Английский

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Clinical Management of Hypertriglyceridemia in the Prevention of Cardiovascular Disease and Pancreatitis

Current Atherosclerosis Reports, Journal Year: 2021, Volume and Issue: 23(11)

Published: Sept. 13, 2021

Language: Английский

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An update on LDL apheresis for nephrotic syndrome

Pediatric Nephrology, Journal Year: 2018, Volume and Issue: 34(10), P. 1655 - 1669

Published: Sept. 14, 2018

Language: Английский

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Cyanate Induces Oxidative Stress Injury and Abnormal Lipid Metabolism in Liver through Nrf2/HO-1

Molecules, Journal Year: 2019, Volume and Issue: 24(18), P. 3231 - 3231

Published: Sept. 5, 2019

Chronic kidney disease (CKD) is problem that has become one of the major issues affecting public health. Extensive clinical data suggests prevalence hyperlipidemia in CKD patients significantly higher than general population. Lipid metabolism disorders can damage renal parenchyma and promote occurrence cardiovascular (CVD). Cyanate a uremic toxin attracted widespread attention recent years. Usually, 0.8% molar concentration urea converted into cyanate, while myeloperoxidase (MPO) catalyzes oxidation thiocyanate to produce cyanate at site inflammation during smoking, inflammation, or exposure environmental pollution. One important physiological functions protein carbonylation, non-enzymatic post-translational modification. Carbamylation reactions on proteins are capable irreversibly changing structure function, resulting pathologic molecular cellular responses. In addition, studies have shown directly vascular tissue by producing large amounts reactive oxygen species (ROS). Oxidative stress leads disorder liver lipid metabolism, which also an mechanism leading cirrhosis fibrosis. However, influence remained unclear. this research, we explored effects oxidative injury abnormal mice HL-7702 cells. results, induced influencing content total cholesterol (TC), high-density lipoprotein (HDL), low-density (LDL), superoxide dismutase (SOD), catalase (CAT) liver. inhibited NF-E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), phosphorylation adenosine 5′monophosphate-activated kinase (AMPK), activated mTOR pathway. cells reduced treating with TBHQ, antioxidant, activator Nrf2. The activity Nrf2 was rehabilitated decreased. conclusion, could induce deposition inhibiting Nrf2/HO-1 pathway, rescued inhibitor

Language: Английский

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Predicting and Defining Steroid Resistance in Pediatric Nephrotic Syndrome Using Plasma Proteomics

Kidney International Reports, Journal Year: 2019, Volume and Issue: 5(1), P. 66 - 80

Published: Sept. 19, 2019

IntroductionNephrotic syndrome (NS) is a characterized by massive proteinuria, edema, hypoalbuminemia, and dyslipidemia. Glucocorticoids (GCs), the primary therapy for >60 years, are ineffective in approximately 50% of adults 20% children. Unfortunately, there no validated biomarkers able to predict steroid-resistant NS (SRNS) or define pathways regulating SRNS.MethodsWe performed proteomic analyses on paired pediatric patient plasma samples obtained both at disease presentation before glucocorticoid initiation after 7 weeks GC identify candidate either steroid resistance treatment critical molecular pathways/targets resistance.ResultsProteomic 15 identified 215 prevalent proteins, including 13 that predicted SRNS treatment, 66 mechanistically differentiated steroid-sensitive (SSNS) from SRNS. Ingenuity Pathway Analyses protein networking approaches further proteins associated with Validation using 37 (24 SSNS/13 SRNS) confirmed vitamin D binding (VDB) APOL1 as strong predictive SRNS, VDB, hemopexin (HPX), adiponectin (ADIPOQ), sex hormone–binding globulin (SHBG), distinguish SSNS. Logistic regression analysis biomarker panel (VDB, ADIPOQ, matrix metalloproteinase 2 [MMP-2]) significant ability (P = 0.003; area under receiver operating characteristic curve 0.78).ConclusionPlasma immunoblotting serial childhood presentation, well targets/pathways clinical resistance.

Language: Английский

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