Lipid Abnormalities in Patients with Chronic Kidney Disease: Implications for the Pathophysiology of Atherosclerosis DOI Creative Commons

William F. Keane,

Joanne E. Tomassini,

David Neff

et al.

Journal of Atherosclerosis and Thrombosis, Journal Year: 2012, Volume and Issue: 20(2), P. 123 - 133

Published: Oct. 24, 2012

Cardiovascular disease is increased in patients with chronic kidney (CKD) and the principle cause of morbidity mortality these patients. In stage 5 CKD, structural changes myocardium have been implicated as cardiovascular processes leading to this increase mortality, while atherosclerotic events including acute myocardial infarction strokes are responsible for approximately 10-15% deaths. Dyslipidemia common CKD usually not characterized by elevated cholesterol levels, except marked proteinuria. Increased triglyceride levels conjunction decreased high-density lipoprotein commonest qualitative abnormality. Characteristically, abnormalities metabolism apolipoprotein (apo) B-containing lipoproteins described, both gut derived (apoB-48) well those produced hepatic synthesis (apoB-100). A decrease enzymatic delipidation reduced receptor removal contribute apo-B-containing particles their remnants (which believed be highly atherogenic). Abnormalities apoA-containing also present lower HDL seen. Qualitative may associated cellular oxidative injury a pro-inflammatory, pro-thrombotic milieu that frequently

Language: Английский

Targeting the transcription factor Nrf2 to ameliorate oxidative stress and inflammation in chronic kidney disease DOI Creative Commons

Stacey Ruiz,

Pablo E. Pérgola, Richard A. Zager

et al.

Kidney International, Journal Year: 2013, Volume and Issue: 83(6), P. 1029 - 1041

Published: Jan. 16, 2013

Language: Английский

Citations

652
HDL and cardiovascular disease: atherogenic and atheroprotective mechanisms DOI
Mohamad Navab, Srinivasa T. Reddy,

Brian J. Van Lenten

et al.

Nature Reviews Cardiology, Journal Year: 2011, Volume and Issue: 8(4), P. 222 - 232

Published: Feb. 8, 2011

Language: Английский

Citations

600
Contribution of impaired Nrf2-Keap1 pathway to oxidative stress and inflammation in chronic renal failure DOI
Hyun Ju Kim, Nosratola D. Vaziri

AJP Renal Physiology, Journal Year: 2009, Volume and Issue: 298(3), P. F662 - F671

Published: Dec. 10, 2009

Oxidative stress and inflammation are constant features major mediators of progression chronic kidney disease (CKD). Nuclear factor erythroid-2-related factor-2 (Nrf2) confers protection against tissue injury by orchestrating antioxidant detoxification responses to oxidative electrophilic stress. While sources in the remnant have been extensively characterized, effect CKD on Nrf2 activation expression its downstream gene products is unknown was investigated. Subgroups male Sprague-Dawley rats were subjected 5/6 nephrectomy or sham operation observed for 6 12 wk. Kidneys then harvested, activity target (antioxidant phase II enzymes) assessed. In addition, key factors involved promoting studied. confirmation earlier studies, with renal failure exhibited increased lipid peroxidation, glutathione depletion, NF-kappaB activation, mononuclear cell infiltration, upregulation monocyte chemoattractant protein-1, NAD(P)H oxidase, cyclooxygenase-2, 12-lipoxygenase pointing inflammation. Despite severe inflammation, (nuclear translocation) mildly reduced at wk markedly wk, whereas repressor Keap1 upregulated genes [catalase, superoxide dismutase, peroxidase, heme oxygenase-1, quinone oxidoreductase, glutamate-cysteine ligase] unchanged significantly diminished Thus compounded conspicuous impairment consequent downregulation enzymes.

Language: Английский

Citations

447
An update on the lipid nephrotoxicity hypothesis DOI
Xiong Z. Ruan, Zac Varghese,

John F. Moorhead

et al.

Nature Reviews Nephrology, Journal Year: 2009, Volume and Issue: 5(12), P. 713 - 721

Published: Oct. 27, 2009

Language: Английский

Citations

303
Uremia Alters HDL Composition and Function DOI Open Access
Michael Holzer, Ruth Birner‐Gruenberger, Tatjana Stojaković

et al.

Journal of the American Society of Nephrology, Journal Year: 2011, Volume and Issue: 22(9), P. 1631 - 1641

Published: July 30, 2011

Functional impairment of HDL may contribute to the excess cardiovascular mortality experienced by patients with renal disease, but effect advanced disease on composition and function is not well understood. Here, we used mass spectrometry biochemical analyses study alterations in proteome lipid isolated from maintenance hemodialysis. We identified a significant increase amount acute phase protein serum amyloid A1, albumin, lipoprotein-associated phospholipase A2, apoC-III composing uremic HDL. Furthermore, contained reduced phospholipid increased triglyceride lysophospholipid. With regard function, these changes impaired ability promote cholesterol efflux macrophages. In summary, altered seems inhibit its cardioprotective properties. Assessing help identify at risk for disease.

Language: Английский

Citations

266
Serum Amyloid A in Uremic HDL Promotes Inflammation DOI Open Access
Thomas Weichhart, Chantal Kopecky, Markus Kubicek

et al.

Journal of the American Society of Nephrology, Journal Year: 2012, Volume and Issue: 23(5), P. 934 - 947

Published: Jan. 27, 2012

Uremia impairs the atheroprotective properties of HDL, but mechanisms underlying why this occurs are unknown. Here, we observed that HDL isolated from healthy individuals inhibited production inflammatory cytokines by peripheral monocytes stimulated with a Toll-like receptor 2 agonist. In contrast, majority patients ESRD did not show anti-inflammatory property; many samples even promoted cytokines. To investigate difference, used shotgun proteomics to identify 49 HDL-associated proteins in uremia-specific pattern. Proteins enriched (ESRD-HDL) included surfactant protein B (SP-B), apolipoprotein C-II, serum amyloid A (SAA), and α-1-microglobulin/bikunin precursor. addition, detected some ESRD-enriched earlier stages CKD. We detect difference oxidation status between uremic patients. Regarding function these proteins, only SAA mimicked ESRD-HDL promoting cytokine production. Furthermore, levels inversely correlated its potency. conclusion, has activities defective as result specific changes molecular composition. These data suggest potential link high inflammation cardiovascular mortality uremia.

Language: Английский

Citations

194
Apolipoprotein A-I (apoA-I) and apoA-I mimetic peptides inhibit tumor development in a mouse model of ovarian cancer DOI Open Access
Feng Su,

Kathy Kozak,

Satoshi Imaizumi

et al.

Proceedings of the National Academy of Sciences, Journal Year: 2010, Volume and Issue: 107(46), P. 19997 - 20002

Published: Nov. 1, 2010

We examined whether reduced levels of Apolipoprotein A-I (apoA-I) in ovarian cancer patients are causal a mouse model. Mice expressing human apoA-I transgene had ( i ) increased survival P < 0.0001) and ii decreased tumor development 0.01), when compared with littermates, following injection epithelial papillary serous adenocarcinoma cells (ID-8 cells). ApoA-I mimetic peptides viability proliferation ID8 cis -platinum–resistant cells, ID-8 cell-mediated burden C57BL/6J mice administered subcutaneously or orally. Serum lysophosphatidic acid, well-characterized modulator cell proliferation, were significantly (>50% control mice, 0.05) that received (administered either orally), suggesting binding removal acid is potential mechanism for the inhibition by peptides, which may serve as previously unexplored class anticancer agents.

Language: Английский

Citations

193
Air pollution and circulating biomarkers of oxidative stress DOI Creative Commons

Ralph J. Delfino,

Norbert Staimer,

Nosratola D. Vaziri

et al.

Air Quality Atmosphere & Health, Journal Year: 2010, Volume and Issue: 4(1), P. 37 - 52

Published: Oct. 12, 2010

Chemical components of air pollutant exposures that induce oxidative stress and subsequent inflammation may be partly responsible for associations cardiovascular morbidity mortality with airborne particulate matter combustion-related gasses. However, epidemiologic evidence regarding this is limited. An exposure-assessment approach to measure the potential particle mixtures because it likely hundreds correlated chemicals are involved in overall effects pollution on health. Oxidative depends composition size distribution, especially ultrafine concentration, transition metals certain semivolatile volatile organic chemicals. For health effects, measuring systemic blood one feasible approach, but there no universal biomarker many target molecules (lipids, proteins, DNA, nitric oxide, etc.), which more or less suitable specific study goals. Concurrent measurement stress, important gene and/or protein expression endogenous antioxidant enzymes they can modify relations between biomarkers pollutants. Conversely, activities these modified by stress. This interplay will determine observed pollutants inflammatory thrombotic mediators related clinical outcomes. Studies needed assess reliability validity biomarkers, evaluate differences various measurements (mass, chemical components, potential), impacts responses relations.

Language: Английский

Citations

169
Oxidative stress and inflammation: Implications in uremia and hemodialysis DOI

Carmelo Libetta,

Vincenzo Sepe, Pasquale Esposito

et al.

Clinical Biochemistry, Journal Year: 2011, Volume and Issue: 44(14-15), P. 1189 - 1198

Published: July 15, 2011

Language: Английский

Citations

166
High Density Lipoprotein and it's Dysfunction DOI Creative Commons
Esin Eren

The Open Biochemistry Journal, Journal Year: 2012, Volume and Issue: 6(1), P. 78 - 93

Published: July 27, 2012

Plasma high-density lipoprotein cholesterol(HDL-C) levels do not predict functionality and composition of lipoprotein(HDL). Traditionally, keeping low-density cholesterol(LDL-C) down HDL-C up have been the goal patients to prevent atherosclerosis that can lead coronary vascular disease(CVD). People think about HDL present in their cholesterol test, but its functional capability.

Language: Английский

Citations

159