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, Jahrgang 39, Nr. 8, 08.2019, S. 1550-1564.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Review › Forschung
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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 -