PMID- 26323267
OWN - NLM
STAT- MEDLINE
DCOM- 20160404
LR  - 20220316
IS  - 1759-5010 (Electronic)
IS  - 1759-5002 (Print)
IS  - 1759-5002 (Linking)
VI  - 13
IP  - 1
DP  - 2016 Jan
TI  - Dysfunctional HDL and atherosclerotic cardiovascular disease.
PG  - 48-60
LID - 10.1038/nrcardio.2015.124 [doi]
AB  - High-density lipoproteins (HDLs) protect against atherosclerosis by removing 
      excess cholesterol from macrophages through the ATP-binding cassette transporter 
      A1 (ABCA1) and ATP-binding cassette transporter G1 (ABCG1) pathways involved in 
      reverse cholesterol transport. Factors that impair the availability of functional 
      apolipoproteins or the activities of ABCA1 and ABCG1 could, therefore, strongly 
      influence atherogenesis. HDL also inhibits lipid oxidation, restores endothelial 
      function, exerts anti-inflammatory and antiapoptotic actions, and exerts 
      anti-inflammatory actions in animal models. Such properties could contribute 
      considerably to the capacity of HDL to inhibit atherosclerosis. Systemic and 
      vascular inflammation has been proposed to convert HDL to a dysfunctional form 
      that has impaired antiatherogenic effects. A loss of anti-inflammatory and 
      antioxidative proteins, perhaps in combination with a gain of proinflammatory 
      proteins, might be another important component in rendering HDL dysfunctional. 
      The proinflammatory enzyme myeloperoxidase induces both oxidative modification 
      and nitrosylation of specific residues on plasma and arterial apolipoprotein A-I 
      to render HDL dysfunctional, which results in impaired ABCA1 macrophage 
      transport, the activation of inflammatory pathways, and an increased risk of 
      coronary artery disease. Understanding the features of dysfunctional HDL or 
      apolipoprotein A-I in clinical practice might lead to new diagnostic and 
      therapeutic approaches to atherosclerosis.
FAU - Rosenson, Robert S
AU  - Rosenson RS
AD  - Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, NY, 
      USA.
FAU - Brewer, H Bryan Jr
AU  - Brewer HB Jr
AD  - Cardiovascular Research Institute, MedStar Research Institute, Washington 
      Hospital Center, Washington, DC, USA.
FAU - Ansell, Benjamin J
AU  - Ansell BJ
AD  - Cardiology Department, David Geffen School of Medicine at UCLA, Los Angeles, CA, 
      USA.
FAU - Barter, Philip
AU  - Barter P
AD  - Centre for Vascular Research at the University of New South Wales, Sydney, 
      Australia.
FAU - Chapman, M John
AU  - Chapman MJ
AD  - National Institute for Health and Medical Research at Pitie-Salpetriere 
      University Hospital, Paris, France.
FAU - Heinecke, Jay W
AU  - Heinecke JW
AD  - Division of Metabolism, Endocrinology and Nutrition, University of Washington, 
      Seattle, WA, USA.
FAU - Kontush, Anatol
AU  - Kontush A
AD  - INSERM-ICAN Research Unit 1166 of the National Institute for Health and Medical 
      Research at Pitie-Salpetriere University Hospital, Paris, France.
FAU - Tall, Alan R
AU  - Tall AR
AD  - Department of Medicine, Columbia University, New York, NY, USA.
FAU - Webb, Nancy R
AU  - Webb NR
AD  - Pharmacology &Nutritional Sciences and Saha Cardiovascular Research Center, 
      University of Kentucky College of Medicine, Lexington, KY, USA.
LA  - eng
GR  - DP3 DK108209/DK/NIDDK NIH HHS/United States
GR  - P30 DK017047/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Review
DEP - 20150901
PL  - England
TA  - Nat Rev Cardiol
JT  - Nature reviews. Cardiology
JID - 101500075
RN  - 0 (ABCA1 protein, human)
RN  - 0 (ATP Binding Cassette Transporter 1)
RN  - 0 (ATP-Binding Cassette Transporters)
RN  - 0 (Apolipoprotein A-I)
RN  - 0 (Lipoproteins, HDL)
SB  - IM
MH  - ATP Binding Cassette Transporter 1/metabolism
MH  - ATP-Binding Cassette Transporters/metabolism
MH  - Apolipoprotein A-I/genetics/metabolism
MH  - Atherosclerosis/*physiopathology
MH  - Diabetes Complications/metabolism
MH  - Humans
MH  - Lipoproteins, HDL/genetics/*metabolism
MH  - Macrophages/metabolism
MH  - Smoking/adverse effects/metabolism
PMC - PMC6245940
MID - NIHMS996165
COIS- Competing interests statement R.S.R., H.B.B., B.J.A., P.B., M.J.C., J.W.H., A.K., 
      and A.R.T. declare competing interests. Please see the article online for 
      details. N.R.W. declares no competing interests.
EDAT- 2015/09/02 06:00
MHDA- 2016/04/05 06:00
PMCR- 2018/11/20
CRDT- 2015/09/02 06:00
PHST- 2015/09/02 06:00 [entrez]
PHST- 2015/09/02 06:00 [pubmed]
PHST- 2016/04/05 06:00 [medline]
PHST- 2018/11/20 00:00 [pmc-release]
AID - nrcardio.2015.124 [pii]
AID - 10.1038/nrcardio.2015.124 [doi]
PST - ppublish
SO  - Nat Rev Cardiol. 2016 Jan;13(1):48-60. doi: 10.1038/nrcardio.2015.124. Epub 2015 
      Sep 1.