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Low-density lipoprotein net charge is a risk factor for atherosclerosis in lupus patients independent of lipid
Marina Rodríguez1,2,3, Montse Guardiola1,2,3, Iris Oliva1,2,3
1Departament de Medicina i Cirurgia, Unitat de Recerca en Lípids i Arteriosclerosi, Universitat Rovira i Virgili, Reus, Spain.
Insights
In systemic lupus erythematosus (SLE), low-density lipoprotein (LDL) net charge is a novel, independent factor contributing to atherosclerosis progression. This finding helps explain residual cardiovascular risk in SLE patients beyond traditional markers.
Area of Science:
- Cardiovascular Research
- Rheumatology
- Lipid Metabolism
Background:
- Systemic lupus erythematosus (SLE) patients experience accelerated atherosclerosis and high cardiovascular disease (CVD) mortality.
- Traditional cardiovascular risk scores often underestimate this risk in SLE patients.
- Residual cardiovascular risk in SLE suggests unidentified contributing factors beyond standard lipid profiles.
Purpose of the Study:
- To investigate the role of lipoprotein net charge in the development and progression of atherosclerosis in SLE patients.
- To determine if net charge is an independent predictor of subclinical atherosclerosis in SLE.
- To identify novel contributors to the heightened cardiovascular risk in SLE.
Main Methods:
- Lipoproteins were isolated from 78 SLE patients and 32 controls using ultracentrifugation.
- Lipoprotein subclass distribution was analyzed by nuclear magnetic resonance spectroscopy.
- Net charges of VLDL, IDL, LDL, and HDL were measured; carotid intima-media thickness (cIMT) assessed atherosclerosis extent.
Main Results:
- All lipoprotein classes showed a negative net charge.
- Negative correlations were observed between IDL and LDL net charge and cIMT in SLE patients (P < 0.05).
- LDL net charge independently explained 4% of cIMT variability, irrespective of traditional risk factors.
Conclusions:
- Low-density lipoprotein (LDL) net charge is a novel, independent contributor to subclinical atherosclerosis in SLE.
- This finding highlights the significant role of IDL and LDL net charge in SLE cardiovascular risk.
- Understanding lipoprotein net charge may refine cardiovascular risk assessment in SLE patients.
Aims:
Patients with systemic lupus erythematosus (SLE) suffer from accelerated atherosclerosis. Their most common cause of death is a cardiovascular disease (CVD), in spite of the presence of moderate lipid alterations and normal cardiovascular risk scores. However, cholesterol still accumulates in the arteries of SLE patients, so we aim to identify additional factors that may help explain the residual risk that exists in these patients. We focus on investigating whether the net charge contributes significantly to both the development and the progression of atherosclerosis in patients with SLE.
Methods:
The lipoproteins from 78 patients with SLE and 32 controls were isolated via sequential ultracentrifugation. Lipoprotein subclasses distributions were analyzed via nuclear magnetic resonance spectroscopy and the net charges of very low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), low-density lipoprotein (LDL) and high-density lipoprotein (HDL) were measured using a Zetasizer Nano-ZS. The degree of atherosclerosis (carotid intima-media thickness [cIMT]) was determined in all the participants.
Results:
Each lipoprotein class exhibited a negative net charge. IDL and LDL net charge correlated negatively with cIMT (r = -0.274, P = 0.034; r = -0.288; P = 0.033, respectively) in patients with SLE. This effect was independent of age, body mass index (BMI), gender, tobacco consumption, high-sensitivity C-reactive protein (hsCRP), lipid concentration and lipoprotein particle number. LDL net charge explained 4% of the cIMT variability among these patients; this contribution was also independent of age, BMI, gender, tobacco consumption, lipids levels, apolipoproteins and hsCRP.
Conclusions:
Low-density lipoprotein net charge may be considered a new independent contributor to subclinical atherosclerosis in SLE patients. The observed relationship was independent of lipid concentrations and extends the prominent role that IDL and LDL play in cardiovascular risk.
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