Platelets, diabetes and myocardial ischemia/reperfusion injury

Russo, Isabella; Penna, Cláudia; Musso, Tiziana; Popara, Jasmin; Alloatti, Giuseppe; Cavalot, Franco; Pagliaro, Pasquale

doi:10.1186/s12933-017-0550-6

Cited by 73 publications

(60 citation statements)

References 113 publications

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“…Although mechanisms underlying the pathogenesis of ischemia/reperfusion injury are particularly complex and multifactorial, there is evidence of interactions between platelet function and ischemia/reperfusion injury, especially in diabetic conditions [151].…”

Section: Atherothrombotic Diseasesmentioning

confidence: 99%

Influence of Cardiometabolic Risk Factors on Platelet Function

Barale

Russo

2020

IJMS

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Platelets are key players in the thrombotic processes. The alterations of platelet function due to the occurrence of metabolic disorders contribute to an increased trend to thrombus formation and arterial occlusion, thus playing a major role in the increased risk of atherothrombotic events in patients with cardiometabolic risk factors. Several lines of evidence strongly correlate metabolic disorders such as obesity, a classical condition of insulin resistance, dyslipidemia, and impaired glucose homeostasis with cardiovascular diseases. The presence of these clinical features together with hypertension and disturbed microhemorrheology are responsible for the prothrombotic tendency due, at least partially, to platelet hyperaggregability and hyperactivation. A number of clinical platelet markers are elevated in obese and type 2 diabetes (T2DM) patients, including the mean platelet volume, circulating levels of platelet microparticles, oxidation products, platelet-derived soluble P-selectin and CD40L, thus contributing to an intersection between obesity, inflammation, and thrombosis. In subjects with insulin resistance and T2DM some defects depend on a reduced sensitivity to mediators-such as nitric oxide and prostacyclin-playing a physiological role in the control of platelet aggregability. Furthermore, other alterations occur only in relation to hyperglycemia. In this review, the main cardiometabolic risk factors, all components of metabolic syndrome involved in the prothrombotic tendency, will be taken into account considering some of the mechanisms involved in the alterations of platelet function resulting in platelet hyperactivation.

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Section: Atherothrombotic Diseasesmentioning

confidence: 99%

Influence of Cardiometabolic Risk Factors on Platelet Function

Barale

Russo

2020

IJMS

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“…The pharmacological cardioprotective strategy to prevent acute global IRI has been tested using different approaches. Over the last few years, multiple pharmacological agents, including volatile anesthetic agents [55], [56], [57], sodium hydrogen exchange inhibitors [58] and statins [59], [60], [61], pharmacological preconditioning [62], [63], anti-oxidants [64], [65], anti-platelets [6], and anti-inflammatory strategies [66], [67], have been explored as potential cardioprotective therapies. However, most preclinical strategies showing cardioprotective effects did not work in clinical settings [68].…”

Section: Pharmacological Targets For Known Ischemia-reperfusion Injurmentioning

confidence: 99%

“…Sphingosine-1-phosphate (S1P) present in the plasma is mainly produced by endothelial cells, platelets, erythrocytes [6], and hepatocytes; other sources include platelets, mast cells, endothelial cells, fibroblasts, and the central nervous system [69], [70], [71], [72]. It is a bioactive lysophospholipid (LP) derived from sphingomyelin and ubiquitous in lipid cell membranes [70] having wide function from apoptosis (pro-apoptotic) to protective (anti-apoptotic) as shown in Figure 2.…”

Section: Sphingosine-1-phosphatementioning

confidence: 99%

“…S1P performs its functions by binding to five G-protein receptors (S1P1, S1P2, S1P3, S1P4, and S1P5) [73]. Recently, researchers have discovered that P2Y12 receptor antagonists, a group of antiplatelet drugs, exert their cardioprotective effect by interacting with some factor in platelets to activate sphingosine kinase [6]. This effect is independent of their anti-thrombotic effect.…”

Section: Sphingosine-1-phosphatementioning

confidence: 99%

“…Lately, it has been discovered that ischemic pre-and post-conditioning affects not only cardiomyocytes but also the coronary vasculature by increasing the synthesis of nitric oxide (NO) and by other mechanisms [5]. Furthermore, circulating blood cells play a vital role in cardioprotection [6], [7]. Platelets and red cells confer cardioprotection by releasing several vesicles, e.g.…”

Section: Introduction Cardioprotectionmentioning

confidence: 99%

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Cardioprotective mechanism of FTY720 in ischemia reperfusion injury

Ahmed

2019

Journal of Basic and Clinical Physiology and Pharmacology

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Cardioprotection is a very challenging area in the field of cardiovascular sciences. Myocardial damage accounts for nearly 50% of injury due to reperfusion, yet there is no effective strategy to prevent this to reduce the burden of heart failure. During last couple of decades, by combining genetic and bimolecular studies, many new drugs have been developed to treat hypertension, heart failure, and cancer. The use of percutaneous coronary intervention has reduced the mortality and morbidity of acute coronary syndrome dramatically. However, there is no standard therapy available that can mitigate cardiac reperfusion injury, which contributes to up to half of myocardial infarcts. Literature shows that the activation of sphingosine receptors, which are G protein-coupled receptors, induces cardioprotection both in vitro and in vivo. The exact mechanism of this protection is not clear yet. In this review, we discuss the mechanism of ischemia reperfusion injury and the role of the FDA-approved sphingosine 1 phosphate drug fingolimod in cardioprotection. Myocardial protection related to ischemia-reperfusion injuryIn recent decades, numerous studies have shown that the myocardial cells possess several coping mechanisms aiming to limit the damage of ischemia/reperfusion. These processes are not limited to the myocardium but Naseer Ahmed is the corresponding author.

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Astragaloside III activates TACE/ADAM17‐dependent anti‐inflammatory and growth factor signaling in endothelial cells in a p38‐dependent fashion

Wang

Yuan

Cao

et al. 2020

Phytotherapy Research

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Astragaloside III (AS-III) is a triterpenoid saponin contained in Astragali Radix and has potent anti-inflammatory effects on vascular endothelial cells; however, underlying mechanisms are unclear. In this study, we provided the first piece of evidence that AS-III induced phosphorylation of TNF-α converting enzyme (TACE) at Thr735 and enhanced its sheddase activity. As a result, AS-III reduced surface TNFR1 level and increased content of sTNFR1 in the culture media, leading to the inhibition of NF-κB signaling pathway and attenuation of downstream cytokine gene expression. Furthermore, AS-III induced TACE-dependent epidermal growth factor receptor (EGFR) transactivation and activation of downstream ERK1/2 and AKT pathways. Finally, AS-III induced activation of p38. Both TACE activation and EGFR transactivation induced by AS-III were significantly inhibited by p38 inhibitor SB203580. Taken together, we concluded that AS-III activates TACE-dependent anti-inflammatory and growth factor signaling in vascular endothelial cells in a p38-dependent fashion, which may contribute to its cardiovascular protective effect. K E Y W O R D SAstragaloside III, epidermal growth factor receptor, p38, TNFR1, TNF-α converting enzyme, vascular endothelial cells

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Platelets, diabetes and myocardial ischemia/reperfusion injury

Cited by 73 publications

References 113 publications

Influence of Cardiometabolic Risk Factors on Platelet Function

Influence of Cardiometabolic Risk Factors on Platelet Function

Cardioprotective mechanism of FTY720 in ischemia reperfusion injury

Astragaloside III activates TACE/ADAM17‐dependent anti‐inflammatory and growth factor signaling in endothelial cells in a p38‐dependent fashion

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