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Reciprocal Multifaceted Interaction Between HDL (High-Density Lipoprotein) and Myocardial Infarction

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Reciprocal Multifaceted Interaction Between HDL (High-Density Lipoprotein) and Myocardial Infarction. / Sposito, Andrei C; de Lima-Junior, José Carlos; Moura, Filipe A; Barreto, Joaquim; Bonilha, Isabella; Santana, Michele; Virginio, Vitor W; Sun, Lufan; Carvalho, Luiz Sergio F; Soares, Alexandre A S; Nadruz, Wilson; Feinstein, Steve B; Nofer, Jerzy-Roch; Zanotti, Ilaria; Kontush, Anatol; Remaley, Alan T.

In: ARTERIOSCL THROM VAS, Vol. 39, No. 8, 08.2019, p. 1550-1564.

Research output: SCORING: Contribution to journal › SCORING: Review article › Research

Harvard

Sposito, AC, de Lima-Junior, JC, Moura, FA, Barreto, J, Bonilha, I, Santana, M, Virginio, VW, Sun, L, Carvalho, LSF, Soares, AAS, Nadruz, W, Feinstein, SB, Nofer, J-R, Zanotti, I, Kontush, A & Remaley, AT 2019, 'Reciprocal Multifaceted Interaction Between HDL (High-Density Lipoprotein) and Myocardial Infarction', ARTERIOSCL THROM VAS, vol. 39, no. 8, pp. 1550-1564. https://doi.org/10.1161/ATVBAHA.119.312880

APA

Sposito, A. C., de Lima-Junior, J. C., Moura, F. A., Barreto, J., Bonilha, I., Santana, M., Virginio, V. W., Sun, L., Carvalho, L. S. F., Soares, A. A. S., Nadruz, W., Feinstein, S. B., Nofer, J-R., Zanotti, I., Kontush, A., & Remaley, A. T. (2019). Reciprocal Multifaceted Interaction Between HDL (High-Density Lipoprotein) and Myocardial Infarction. ARTERIOSCL THROM VAS, 39(8), 1550-1564. https://doi.org/10.1161/ATVBAHA.119.312880

Vancouver

Sposito AC, de Lima-Junior JC, Moura FA, Barreto J, Bonilha I, Santana M et al. Reciprocal Multifaceted Interaction Between HDL (High-Density Lipoprotein) and Myocardial Infarction. ARTERIOSCL THROM VAS. 2019 Aug;39(8):1550-1564. https://doi.org/10.1161/ATVBAHA.119.312880

Bibtex

@article{3fcc43c311cf4bfba3f4070a89c4ba26,
title = "Reciprocal Multifaceted Interaction Between HDL (High-Density Lipoprotein) and Myocardial Infarction",
abstract = "Despite decades of therapeutic advances, myocardial infarction remains a leading cause of death worldwide. Recent studies have identified HDLs (high-density lipoproteins) as a potential candidate for mitigating coronary ischemia/reperfusion injury via a broad spectrum of signaling pathways. HDL ligands, such as S1P (sphingosine-1-phosphate), Apo (apolipoprotein) A-I, clusterin, and miRNA, may influence the opening of the mitochondrial channel, insulin sensitivity, and production of vascular autacoids, such as NO, prostacyclin, and endothelin-1. In parallel, antioxidant activity and sequestration of oxidized molecules provided by HDL can attenuate the oxidative stress that triggers ischemia/reperfusion. Nevertheless, during myocardial infarction, oxidation and the capture of oxidized and proinflammatory molecules generate large phenotypic and functional changes in HDL, potentially limiting its beneficial properties. In this review, new findings from cellular and animal models, as well as from clinical studies, will be discussed to describe the cardioprotective benefits of HDL on myocardial infarction. Furthermore, mechanisms by which HDL modulates cardiac function and potential strategies to mitigate postmyocardial infarction risk damage by HDL will be detailed throughout the review.",
keywords = "Animals, Cholesterol/metabolism, Endothelial Cells/physiology, Glucose/metabolism, Homeostasis, Humans, Lipoproteins, HDL/blood, Lysophospholipids/physiology, Myocardial Infarction/prevention & control, Oxidative Stress, Signal Transduction/physiology, Sphingosine/analogs & derivatives",
author = "Sposito, {Andrei C} and {de Lima-Junior}, {Jos{\'e} Carlos} and Moura, {Filipe A} and Joaquim Barreto and Isabella Bonilha and Michele Santana and Virginio, {Vitor W} and Lufan Sun and Carvalho, {Luiz Sergio F} and Soares, {Alexandre A S} and Wilson Nadruz and Feinstein, {Steve B} and Jerzy-Roch Nofer and Ilaria Zanotti and Anatol Kontush and Remaley, {Alan T}",
year = "2019",
month = aug,
doi = "10.1161/ATVBAHA.119.312880",
language = "English",
volume = "39",
pages = "1550--1564",
journal = "ARTERIOSCL THROM VAS",
issn = "1079-5642",
publisher = "Lippincott Williams and Wilkins",
number = "8",

}

RIS

TY - JOUR

T1 - Reciprocal Multifaceted Interaction Between HDL (High-Density Lipoprotein) and Myocardial Infarction

AU - Sposito, Andrei C

AU - de Lima-Junior, José Carlos

AU - Moura, Filipe A

AU - Barreto, Joaquim

AU - Bonilha, Isabella

AU - Santana, Michele

AU - Virginio, Vitor W

AU - Sun, Lufan

AU - Carvalho, Luiz Sergio F

AU - Soares, Alexandre A S

AU - Nadruz, Wilson

AU - Feinstein, Steve B

AU - Nofer, Jerzy-Roch

AU - Zanotti, Ilaria

AU - Kontush, Anatol

AU - Remaley, Alan T

PY - 2019/8

Y1 - 2019/8

N2 - Despite decades of therapeutic advances, myocardial infarction remains a leading cause of death worldwide. Recent studies have identified HDLs (high-density lipoproteins) as a potential candidate for mitigating coronary ischemia/reperfusion injury via a broad spectrum of signaling pathways. HDL ligands, such as S1P (sphingosine-1-phosphate), Apo (apolipoprotein) A-I, clusterin, and miRNA, may influence the opening of the mitochondrial channel, insulin sensitivity, and production of vascular autacoids, such as NO, prostacyclin, and endothelin-1. In parallel, antioxidant activity and sequestration of oxidized molecules provided by HDL can attenuate the oxidative stress that triggers ischemia/reperfusion. Nevertheless, during myocardial infarction, oxidation and the capture of oxidized and proinflammatory molecules generate large phenotypic and functional changes in HDL, potentially limiting its beneficial properties. In this review, new findings from cellular and animal models, as well as from clinical studies, will be discussed to describe the cardioprotective benefits of HDL on myocardial infarction. Furthermore, mechanisms by which HDL modulates cardiac function and potential strategies to mitigate postmyocardial infarction risk damage by HDL will be detailed throughout the review.

AB - Despite decades of therapeutic advances, myocardial infarction remains a leading cause of death worldwide. Recent studies have identified HDLs (high-density lipoproteins) as a potential candidate for mitigating coronary ischemia/reperfusion injury via a broad spectrum of signaling pathways. HDL ligands, such as S1P (sphingosine-1-phosphate), Apo (apolipoprotein) A-I, clusterin, and miRNA, may influence the opening of the mitochondrial channel, insulin sensitivity, and production of vascular autacoids, such as NO, prostacyclin, and endothelin-1. In parallel, antioxidant activity and sequestration of oxidized molecules provided by HDL can attenuate the oxidative stress that triggers ischemia/reperfusion. Nevertheless, during myocardial infarction, oxidation and the capture of oxidized and proinflammatory molecules generate large phenotypic and functional changes in HDL, potentially limiting its beneficial properties. In this review, new findings from cellular and animal models, as well as from clinical studies, will be discussed to describe the cardioprotective benefits of HDL on myocardial infarction. Furthermore, mechanisms by which HDL modulates cardiac function and potential strategies to mitigate postmyocardial infarction risk damage by HDL will be detailed throughout the review.

KW - Animals

KW - Cholesterol/metabolism

KW - Endothelial Cells/physiology

KW - Glucose/metabolism

KW - Homeostasis

KW - Humans

KW - Lipoproteins, HDL/blood

KW - Lysophospholipids/physiology

KW - Myocardial Infarction/prevention & control

KW - Oxidative Stress

KW - Signal Transduction/physiology

KW - Sphingosine/analogs & derivatives

U2 - 10.1161/ATVBAHA.119.312880

DO - 10.1161/ATVBAHA.119.312880

M3 - SCORING: Review article

C2 - 31189429

VL - 39

SP - 1550

EP - 1564

JO - ARTERIOSCL THROM VAS

JF - ARTERIOSCL THROM VAS

SN - 1079-5642

IS - 8

ER -