High-density lipoproteins and apolipoprotein A-I improve stent biocompatibility recent evidence from experimental models and clinical studies

Laura Z. Vanags, Nathan K.P. Wong, Stephen J. Nicholls, Christina A. Bursill

Research output: Contribution to journalReview article

2 Citations (Scopus)

Abstract

Revascularization because of coronary artery disease is commonly achieved by percutaneous coronary intervention with stent deployment. Refinement in interventional techniques, major improvements in stent design (particularly drug-eluting stents), and adjunctive pharmacotherapy with dual antiplatelet regimens have led to marked reductions in the overall rates of stent failure. However, even with the advancements made in the latest generation of drug-eluting stents, unresolved biological problems persist including delayed re-endothelialization and neoatherosclerosis, which can promote late expansion of the neointima and late stent thrombosis. Novel strategies are still needed beyond what is currently available to specifically address the pathobiological processes that underpin the residual risk for adverse clinical events. This review focuses on the emerging evidence that HDL (high-density lipoproteins) and its main apo (apolipoprotein), apoA-I, exhibit multiple vascular biological functions that are associated with an improvement in stent biocompatibility. HDL/apoA-I have recently been shown to inhibit in-stent restenosis in animal models of stenting and suppress smooth muscle cell proliferation in in vitro studies. Reconstituted HDL also promotes endothelial cell migration, endothelial progenitor cell mobilization, and re-endothelialization. Furthermore, reconstituted HDL decreases platelet activation and HDL cholesterol is inversely associated with the risk of thrombosis. Finally, reconstituted HDL/apoA-I suppresses key inflammatory mechanisms that initiate in-stent neoatherosclerosis and can efflux cholesterol from plaque macrophages, an important function of HDLs that prevents plaque progression. These unique multifunctional effects of HDL/apoA-I suggest that, if translated appropriately, have the potential to improve stent biocompatibility. This may provide an alternate and more efficacious therapeutic pathway for the translation of HDL.

LanguageEnglish
Pages1691-1701
Number of pages11
JournalArteriosclerosis, Thrombosis, and Vascular Biology
Volume38
Issue number8
DOIs
Publication statusPublished - 1 Jan 2018

Keywords

  • Apolipoprotein A-I
  • Coronary artery disease
  • Hyperplasia
  • Stents
  • Thrombosis

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

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title = "High-density lipoproteins and apolipoprotein A-I improve stent biocompatibility recent evidence from experimental models and clinical studies",
abstract = "Revascularization because of coronary artery disease is commonly achieved by percutaneous coronary intervention with stent deployment. Refinement in interventional techniques, major improvements in stent design (particularly drug-eluting stents), and adjunctive pharmacotherapy with dual antiplatelet regimens have led to marked reductions in the overall rates of stent failure. However, even with the advancements made in the latest generation of drug-eluting stents, unresolved biological problems persist including delayed re-endothelialization and neoatherosclerosis, which can promote late expansion of the neointima and late stent thrombosis. Novel strategies are still needed beyond what is currently available to specifically address the pathobiological processes that underpin the residual risk for adverse clinical events. This review focuses on the emerging evidence that HDL (high-density lipoproteins) and its main apo (apolipoprotein), apoA-I, exhibit multiple vascular biological functions that are associated with an improvement in stent biocompatibility. HDL/apoA-I have recently been shown to inhibit in-stent restenosis in animal models of stenting and suppress smooth muscle cell proliferation in in vitro studies. Reconstituted HDL also promotes endothelial cell migration, endothelial progenitor cell mobilization, and re-endothelialization. Furthermore, reconstituted HDL decreases platelet activation and HDL cholesterol is inversely associated with the risk of thrombosis. Finally, reconstituted HDL/apoA-I suppresses key inflammatory mechanisms that initiate in-stent neoatherosclerosis and can efflux cholesterol from plaque macrophages, an important function of HDLs that prevents plaque progression. These unique multifunctional effects of HDL/apoA-I suggest that, if translated appropriately, have the potential to improve stent biocompatibility. This may provide an alternate and more efficacious therapeutic pathway for the translation of HDL.",
keywords = "Apolipoprotein A-I, Coronary artery disease, Hyperplasia, Stents, Thrombosis",
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High-density lipoproteins and apolipoprotein A-I improve stent biocompatibility recent evidence from experimental models and clinical studies. / Vanags, Laura Z.; Wong, Nathan K.P.; Nicholls, Stephen J.; Bursill, Christina A.

In: Arteriosclerosis, Thrombosis, and Vascular Biology, Vol. 38, No. 8, 01.01.2018, p. 1691-1701.

Research output: Contribution to journalReview article

TY - JOUR

T1 - High-density lipoproteins and apolipoprotein A-I improve stent biocompatibility recent evidence from experimental models and clinical studies

AU - Vanags, Laura Z.

AU - Wong, Nathan K.P.

AU - Nicholls, Stephen J.

AU - Bursill, Christina A.

PY - 2018/1/1

Y1 - 2018/1/1

N2 - Revascularization because of coronary artery disease is commonly achieved by percutaneous coronary intervention with stent deployment. Refinement in interventional techniques, major improvements in stent design (particularly drug-eluting stents), and adjunctive pharmacotherapy with dual antiplatelet regimens have led to marked reductions in the overall rates of stent failure. However, even with the advancements made in the latest generation of drug-eluting stents, unresolved biological problems persist including delayed re-endothelialization and neoatherosclerosis, which can promote late expansion of the neointima and late stent thrombosis. Novel strategies are still needed beyond what is currently available to specifically address the pathobiological processes that underpin the residual risk for adverse clinical events. This review focuses on the emerging evidence that HDL (high-density lipoproteins) and its main apo (apolipoprotein), apoA-I, exhibit multiple vascular biological functions that are associated with an improvement in stent biocompatibility. HDL/apoA-I have recently been shown to inhibit in-stent restenosis in animal models of stenting and suppress smooth muscle cell proliferation in in vitro studies. Reconstituted HDL also promotes endothelial cell migration, endothelial progenitor cell mobilization, and re-endothelialization. Furthermore, reconstituted HDL decreases platelet activation and HDL cholesterol is inversely associated with the risk of thrombosis. Finally, reconstituted HDL/apoA-I suppresses key inflammatory mechanisms that initiate in-stent neoatherosclerosis and can efflux cholesterol from plaque macrophages, an important function of HDLs that prevents plaque progression. These unique multifunctional effects of HDL/apoA-I suggest that, if translated appropriately, have the potential to improve stent biocompatibility. This may provide an alternate and more efficacious therapeutic pathway for the translation of HDL.

AB - Revascularization because of coronary artery disease is commonly achieved by percutaneous coronary intervention with stent deployment. Refinement in interventional techniques, major improvements in stent design (particularly drug-eluting stents), and adjunctive pharmacotherapy with dual antiplatelet regimens have led to marked reductions in the overall rates of stent failure. However, even with the advancements made in the latest generation of drug-eluting stents, unresolved biological problems persist including delayed re-endothelialization and neoatherosclerosis, which can promote late expansion of the neointima and late stent thrombosis. Novel strategies are still needed beyond what is currently available to specifically address the pathobiological processes that underpin the residual risk for adverse clinical events. This review focuses on the emerging evidence that HDL (high-density lipoproteins) and its main apo (apolipoprotein), apoA-I, exhibit multiple vascular biological functions that are associated with an improvement in stent biocompatibility. HDL/apoA-I have recently been shown to inhibit in-stent restenosis in animal models of stenting and suppress smooth muscle cell proliferation in in vitro studies. Reconstituted HDL also promotes endothelial cell migration, endothelial progenitor cell mobilization, and re-endothelialization. Furthermore, reconstituted HDL decreases platelet activation and HDL cholesterol is inversely associated with the risk of thrombosis. Finally, reconstituted HDL/apoA-I suppresses key inflammatory mechanisms that initiate in-stent neoatherosclerosis and can efflux cholesterol from plaque macrophages, an important function of HDLs that prevents plaque progression. These unique multifunctional effects of HDL/apoA-I suggest that, if translated appropriately, have the potential to improve stent biocompatibility. This may provide an alternate and more efficacious therapeutic pathway for the translation of HDL.

KW - Apolipoprotein A-I

KW - Coronary artery disease

KW - Hyperplasia

KW - Stents

KW - Thrombosis

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U2 - 10.1161/ATVBAHA.118.310788

DO - 10.1161/ATVBAHA.118.310788

M3 - Review article

VL - 38

SP - 1691

EP - 1701

JO - Arteriosclerosis, thrombosis, and vascular biology

T2 - Arteriosclerosis, thrombosis, and vascular biology

JF - Arteriosclerosis, thrombosis, and vascular biology

SN - 1079-5642

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ER -