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Subpopulations of High-Density Lipoprotein: Friends or Foes in Cardiovascular Disease Risk in Chronic Kidney Disease?

期刊

BIOMEDICINES
卷 9, 期 5, 页码 -

出版社

MDPI
DOI: 10.3390/biomedicines9050554

关键词

HDL subpopulations; cardiovascular disease risk; chronic kidney disease; inflammation; oxidative stress; HDL functionality

资金

  1. FCT
  2. CCDR-C/CENTRO2020/Portugal2020 [UIDP/04539/2020, PTDC/SAU-NUT/31712/2017, PO-CI-01-0145-FEDER-007440, CENTRO-01-0145-FEDER-000012-HealthyAging2020]
  3. Applied Molecular Biosciences Unit (UCIBIO) - FCT [UIDP/04378/2020, UIDB/04378/2020]
  4. North Portugal Regional Coordination and Development Commission (CCDR-N)/NORTE2020/Portugal 2020 [Norte-01-0145-FEDER-000024]
  5. FEDER/COMPETE

向作者/读者索取更多资源

Dyslipidemia is a major risk factor for cardiovascular disease in chronic kidney disease patients, but the role of HDL in this population is complex and poorly understood. The unique proteome and lipid composition of large HDL in CKD patients may impair their cholesterol efflux capacity, contributing to a paradoxical coexistence of increased large HDL and enhanced risk for CVD events. Additional research is needed to better understand how these changes in HDL functionality impact cardiovascular risk in CKD patients.
Dyslipidemia is a major traditional risk factor for cardiovascular disease (CVD) in chronic kidney disease (CKD) patients, although the altered lipid profile does not explain the number and severity of CVD events. High-density lipoprotein (HDL) is a heterogeneous (size, composition, and functionality) population of particles with different atherogenic or atheroprotective properties. HDL-cholesterol concentrations per se may not entirely reflect a beneficial or a risk profile for CVD. Large HDL in CKD patients may have a unique proteome and lipid composition, impairing their cholesterol efflux capacity. This lack of HDL functionality may contribute to the paradoxical coexistence of increased large HDL and enhanced risk for CVD events. Moreover, CKD is associated with inflammation, oxidative stress, diabetes, and/or hypertension that are able to interfere with the anti-inflammatory, antioxidative, and antithrombotic properties of HDL subpopulations. How these changes interfere with HDL functions in CKD is still poorly understood. Further studies are warranted to fully clarify if different HDL subpopulations present different functionalities and/or atheroprotective effects. To achieve this goal, the standardization of techniques would be valuable.

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