Platelet acetyl-CoA carboxylase phosphorylation: A risk stratification marker that reveals platelet-lipid interplay in coronary artery disease patients

Kautbally, Shakeel; Lepropre, Sophie; Lerigoleur, A.; Ginion, Audrey; Ambroise, Jérôme; Meester, Carole de; Zouaoui, K.; Giera, Martin; Guigas, Bruno; Pouleur, Anne-Catherine; Oury, Cécile; Bertrand, Luc; Horman, Sandrine; Beauloye, Christophe

doi:10.1016/j.acvdsp.2019.02.010

Cited by 4 publications

(4 citation statements)

References 19 publications

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“…However, many studies have been conducted to find out the role of the ACC in several diseases. [14][15][16] A study demonstrated that reduction of cardiac ACC2 led to a significant decrease in cardiac MCA, which is considered as a substrate for the synthesis of FA. 17 Inhibiting MCA production activates carnitine Palmitoyltranseferase 1CPT-1.…”

Section: Resultsmentioning

confidence: 99%

Relation between Acetyl-CoA Carboxylase with some Biochemical Variables in Iraqi Men with Acute Myocardial Infarction and Diabetes

Abdulkareem¹,

Ali²,

Mohamad³

2022

IJDDT

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Background: Acute myocardial infarction (AMI) is a widespread cause of death in numerous parts of the world. Many factors raise the risk of myocardial infarction (MI). One of the most of it is atherosclerosis, caused by many factors such as Hyperlipidemia. Acetyl-CoA carboxylase (ACC) is the key regulatory enzyme in fatty acid synthesis. The disorder of lipid metabolism is one of the characteristics of diabetes, which is considered a risk factor for MI. Therefore, the activity ACC was estimated in patients with AMI and Diabetes. Method: The study included estimation of ACC activity and correlated with other biochemical variables such as Troponin T(cTnT), C-reactive protein (CRP), glucose‚ lipid profile, electrolytes [Sodium (Na⁺), Potassium(K⁺), Chloride (Cl⁻)]‚ urea and creatinine (Crea.), and evaluation of body mass index (BMI) effect in serum of 60 patients with AMI and diabetes compared with 30 serum from apparently healthy individuals as a control group, both groups are of males with an average age (25–60 years). Results and Conclusions: Results showed a significant increase in levels of ACC, cTnT, CRP, Glucose, and Lipid profile except for high-density lipoprotein – cholesterol (HDL-C) and urea, while a significant decrease with Na⁺and K⁺ also a non-significant variation was observed with Cl⁻ and creatinine in AMI and diabetes patients compared to control group.

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Section: Resultsmentioning

confidence: 99%

Relation between Acetyl-CoA Carboxylase with some Biochemical Variables in Iraqi Men with Acute Myocardial Infarction and Diabetes

Abdulkareem¹,

Ali²,

Mohamad³

2022

IJDDT

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“…Scavenger receptor-linked signalling proteins as biomarkers. A recent report indicated that the phosphorylation of acethyl-CoA carboxylase (ACC) in platelets, potentially downstream of CD36, was causally linked to poorer outcomes in ACS patients [ 156 ]. This is the first example of a scavenger receptor-linked biomarker for thrombotic risk and could open up the possibility of further specific early appearance biomarkers for preventive of thrombosis.…”

Section: Discussionmentioning

confidence: 99%

Oxidised Low-Density Lipoprotein-Induced Platelet Hyperactivity—Receptors and Signalling Mechanisms

Berger

Naseem

2022

IJMS

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Dyslipidaemia leads to proatherogenic oxidative lipid stress that promotes vascular inflammation and thrombosis, the pathologies that underpin myocardial infarction, stroke, and deep vein thrombosis. These prothrombotic states are driven, at least in part, by platelet hyperactivity, and they are concurrent with the appearancxe of oxidatively modified low-density lipoproteins (LDL) in the circulation. Modified LDL are heterogenous in nature but, in a general sense, constitute a prototype circulating transporter for a plethora of oxidised lipid epitopes that act as danger-associated molecular patterns. It is well-established that oxidatively modified LDL promote platelet activation and arterial thrombosis through a number of constitutively expressed scavenger receptors, which transduce atherogenic lipid stress to a complex array of proactivatory signalling pathways in the platelets. Stimulation of these signalling events underlie the ability of modified LDL to induce platelet activation and blunt platelet inhibitory pathways, as well as promote platelet-mediated coagulation. Accumulating evidence from patients at risk of arterial thrombosis and experimental animal models of disease suggest that oxidised LDL represents a tangible link between the dyslipidaemic environment and increased platelet activation. The aim of this review is to summarise recent advances in our understanding of the pro-thrombotic signalling events induced in platelets by modified LDL ligation, describe the contribution of individual platelet scavenger receptors, and highlight potential future challenges of targeting these pathways.

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“…While the impact of DNL on these lipid alterations has not been extensively studied to date, it is noteworthy that it appears to be influenced by coronary artery disease (CAD). AMPK-mediated phosphorylation of ACC has been proposed as a potential risk stratification marker, given its observed increase in the platelets of CAD patients and strong association with acute coronary events [ 57 ].…”

Section: Platelet Acetyl-coa Carboxylase and Lipids In Pathologiesmentioning

confidence: 99%

Platelet lipidomics and de novo lipogenesis: impact on health and disease

Pirotton,

de Cartier d’Yves,

Bertrand

et al. 2024

Current Opinion in Hematology

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Purpose of review Lipids play vital roles in platelet structure, signaling, and metabolism. In addition to capturing exogenous lipids, platelets possess the capacity for de novo lipogenesis, regulated by acetyl-coA carboxylase 1 (ACC1). This review aims to cover the critical roles of platelet de novo lipogenesis and lipidome in platelet production, function, and diseases. Recent findings Upon platelet activation, approximately 20% of the platelet lipidome undergoes significant modifications, primarily affecting arachidonic acid-containing species. Multiple studies emphasize the impact of de novo lipogenesis, with ACC1 as key player, on platelet functions. Mouse models suggest the importance of the AMPK-ACC1 axis in regulating platelet membrane arachidonic acid content, associated with TXA2 secretion, and thrombus formation. In human platelets, ACC1 inhibition leads to reduced platelet reactivity. Remodeling of the platelet lipidome, alongside with de novo lipogenesis, is also crucial for platelet biogenesis. Disruptions in the platelet lipidome are observed in various pathological conditions, including cardiovascular and inflammatory diseases, with associations between these alterations and shifts in platelet reactivity highlighted. Summary The platelet lipidome, partially regulated by ACC-driven de novo lipogenesis, is indispensable for platelet production and function. It is implicated in various pathological conditions involving platelets.

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Platelet acetyl-CoA carboxylase phosphorylation: A risk stratification marker that reveals platelet-lipid interplay in coronary artery disease patients

Cited by 4 publications

References 19 publications

Relation between Acetyl-CoA Carboxylase with some Biochemical Variables in Iraqi Men with Acute Myocardial Infarction and Diabetes

Relation between Acetyl-CoA Carboxylase with some Biochemical Variables in Iraqi Men with Acute Myocardial Infarction and Diabetes

Oxidised Low-Density Lipoprotein-Induced Platelet Hyperactivity—Receptors and Signalling Mechanisms

Platelet lipidomics and de novo lipogenesis: impact on health and disease

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