Dyslipidemia Biomarkers | Biomarker Commons

Dyslipidemia Biomarkers

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Stromal cell-derived factor-1α as a novel biomarker for hyperlipidemia.

Wed, 05/22/2013
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Stromal cell-derived factor-1α as a novel biomarker for hyperlipidemia.

Tohoku J Exp Med. 2012;228(4):355-63

Authors: Li SL, Lin W, Zhang Y, Zheng ZC, Liu LJ, Fu H, Liu J, Wang GD, Chen SY, Feng LH

Abstract
Stromal cell-derived factor-1 (SDF-1) is expressed in a wide variety of organs, such as heart, and plays a pivotal role in the mobilization of hematopoietic stem and progenitor cells in bone marrow. SDF-1α, a common subtype of SDF-1, may control hematopoiesis and angiogenesis, but its role in the pathogenesis of hyperlipidemia is unknown. The aim of this study was to determine the role of SDF-1α in the pathogenesis of hyperlipidemia. First, log-transformed SDF-1α serum levels (logSDF-1α) were significantly higher in male patients with borderline high lipid profile (BHLP; n=28; 2.15±0.08 ng/ml) compared to control subjects (n=37; 1.94±0.06 ng/ml; P<0.01). The logSDF-1α in male patients with high lipid profile (HLP; n=33; 1.95±0.08 ng/ml) were lower than BHLP patients (P<0.01). The logSDF-1α was positively associated with HDL-C only in female patients (n=125; r=0.379, P=0.016). These results suggest the different pathophysiology in male and female patients with hyperlipidemia. Moreover, flow cytometry analysis showed that expression of the SDF-1α receptor, CXC-chemokine receptor 4, was lower in peripheral blood mononuclear cells of patients with BHLP (n=10) and HLP (n=10), compared to control subjects (n=10; P<0.001). Lastly, peripheral blood leukocyte, neutrophil and lymphocyte counts were higher in BHLP patients (n=62; P<0.05). Taken together, we suggest SDF-1α as a biomarker of hyperlipidemia that may be helpful to uncover the pathogenesis of hyperlipidemia.

PMID: 23149815 [PubMed - indexed for MEDLINE]

Clinical assessment and management of dyslipidemia in patients with chronic kidney disease.

Tue, 04/16/2013
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Clinical assessment and management of dyslipidemia in patients with chronic kidney disease.

Clin Exp Nephrol. 2012 Aug;16(4):522-9

Authors: Nitta K

Abstract
Chronic kidney disease (CKD) is a common cause of cardiovascular disease (CVD). Several factors contribute to the onset and progression of atherosclerosis and CVD in CKD patients. Most of the cases of coronary heart disease in the general population can be explained by traditional risk factors, whereas non-traditional risk factors, including oxidative stress, anemia, inflammation, malnutrition, vascular calcification, and endothelial dysfunction, have been proposed to play a central role in the pathogenesis of CVD in CKD patients. However, the precise mechanism of CVD initiation in CKD patients remains unclear. Lipid-lowering therapies may decrease proteinuria, and increase or maintain renal function. Because the serum levels of triglyceride-rich lipoproteins are increased in CKD patients, particularly in advanced stages, the serum non-HDL cholesterol level may be a better biomarker of dyslipidemia than the serum LDL cholesterol level in this population. A meta-analysis showed that statin therapy was associated with decreased albuminuria in comparison with a placebo. Moreover, lipid-lowering therapy with statins is effective in reducing the risk of CVD in the early stages of CKD, whereas the benefit of statins in patients with end-stage renal disease may be limited.

PMID: 22722878 [PubMed - indexed for MEDLINE]

[Differential plasma protein profiles in patients with hyperlipidemia & atherosclerosis of different patterns of phlegm-stasis syndrome].

Tue, 04/02/2013
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[Differential plasma protein profiles in patients with hyperlipidemia & atherosclerosis of different patterns of phlegm-stasis syndrome].

Zhongguo Zhong Xi Yi Jie He Za Zhi. 2010 May;30(5):482-7

Authors: Liu JL, Song JN, Yan L

Abstract
OBJECTIVE: To investigate the differential plasma protein profiles in patients with hyperlipidemia & atherosclerosis (H&A) of different patterns of phlegm-stasis syndrome (PSS) for seeking their biomarker proteins.
METHODS: Two-dimensional gel electrophoresis and gel screening graphical analysis were performed on plasma proteins got from 146 patients; corresponding protein spots were fetched from the gel for two-stage mass-spectrometric analysis by quadruple time-of-flight mass spectrometry; then the differential proteins for PSS were discriminated by Fisher discriminate analysis.
RESULTS: Excepting two uncertain proteins, 7 differential proteins were screened out from the 11 differentially expressed plasma protein spots with variability over 100% in the inter-block matching. Classic analysis found that haptoglobin precursor and fibrinogen gamma chain were possibly the plasma biomarker proteins for H & A; fibrinogen beta chain and apolipoprotein A-I precursor were that set apart PSS from non-PSS; fibrinogen gamma chain, albumin and apolipoprotein A-I precursor were for phlegm syndrome; haptoglobin precursor, adrenomedullin binding protein precursor, albumin and complement component C4 were for stasis syndrome; albumin and adrenomedullin binding protein precursor were for the phlegm-stasis mutual blocking syndrome. Moreover, the above mentioned expressions of possible marker proteins had their own special rule of changing in the transforming progress of PSS.
CONCLUSION: This study reported, for the first time, the existence of evident variation of functional protein constitution in different patterns of PSS, and definite compatibility being detected in some functional proteins, which may be the marker proteins for making diagnosis and prognosis of PSS in H&A. Besides, preliminary proof for the transformation of PSS has gained at the functional protein level.

PMID: 20690209 [PubMed - indexed for MEDLINE]