The role of platelets in inflammation

Thomas, Mark R.; Storey, Robert F.

doi:10.1160/th14-12-1067

Cited by 380 publications

(188 citation statements)

References 128 publications

(133 reference statements)

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“…After atherosclerotic plaque rupture, complex cross talk between platelets and leukocytes amplifies the development of a thrombus and the initiation of systemic inflammation. 28,29 The thrombus may occlude the coronary artery, resulting in myocardial ischemia, which leads to the release of damageassociated molecular patterns, such as heat shock proteins. Damage-associated molecular patterns trigger leukocyte release of proinflammatory cytokines, which drives systemic inflammation and is characterized by increased levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and C-reactive protein (CRP; Table 2).…”

Section: Inflammation-related Risk Factorsmentioning

confidence: 99%

Novel Risk Markers and Risk Assessments for Cardiovascular Disease

Thomas

Lip

2017

Circulation Research

110

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Abstract:The use of risk markers has transformed cardiovascular medicine, exemplified by the routine assessment of troponin, for both diagnosis and assessment of prognosis in patients with chest pain. Clinical risk factors form the basis for risk assessment of cardiovascular disease and the addition of biochemical, cellular, and imaging parameters offers further refinement. Identifying novel risk factors may allow greater risk stratification and a steady, but gradual progression toward precision medicine. Indeed, the generation of data in this area of research is explosive and when combined with new technologies and techniques provides the potential for more refined, targeted approaches to cardiovascular medicine. Although discussing the most recent developments in this field, this review article aims to strike a balance between novelty and validity by focusing on recent large samplesize studies that have been validated in a separate cohort in most cases. Risk markers related to atherosclerosis, thrombosis, inflammation, cardiac injury, and fibrosis are introduced in the context of their pathophysiology. Rapidly developing new areas, such as assessment of micro-RNA, are also explored. Subsequently the prognostic ability of these risk markers in coronary artery disease, heart failure, and atrial fibrillation is discussed in detail. ( addition to these roles in the pathogenesis of coronary artery disease, lipid-related molecules have been identified to be markers of inflammation and oxidative stress (Table 1). Thrombosis-Related Risk MarkersAfter atherosclerotic plaque rupture, platelets adhere to exposed subendothelial components, such as collagen and von Willebrand factor, which promotes platelet activation and aggregation. 10 In addition, platelet activation is potentiated by exposure to released soluble agonists, such as thrombin and ADP.10 Activated platelets then further release ADP, which acts on platelet P2Y 12 ADP receptors and has a central role in amplifying the response of platelets to the initial stimulus. 10 Platelet reactivity to various agonists, including ADP, has been studied extensively in the context of acute coronary syndrome (ACS; Table 2). 11 The VerifyNow and Multiplate pointof-care tests allow for the measurement of platelet aggregation in response to stimulation, and it has been shown that high platelet reactivity is associated with adverse cardiovascular events. 26 Platelet microparticles are released on platelet activation, and their role in cardiovascular disease is an area of active investigation (Table 2). 15 Circulating microparticles are released from cells undergoing activation or apoptosis and are a type of small plasma membrane vesicle that retain defined properties from their original cell lineage. 15 Platelet activation and aggregation lead to the activation of the coagulation cascade and the formation of a stable crosslinked fibrin clot. The balance between prothrombotic factors and endogenous fibrinolysis determines whether the thrombus propagates or instead proceeds to dis...

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Section: Inflammation-related Risk Factorsmentioning

confidence: 99%

Novel Risk Markers and Risk Assessments for Cardiovascular Disease

Thomas

Lip

2017

Circulation Research

110

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“…acetylsalicylic acid) given its primary anti-aggregatory mechanism of action. However, with the emerging evidence on role of platelets in inflammatory reactions and immunomodulation, platelet inhibition with aspirin has been found to also elicit also anti-inflammatory effects [7, 8, 9•, 10]. Moreover, aspirin was found to work as acetylating agent with a range of beneficial effects on vascular endothelium beyond platelet inhibition.…”

Section: Introductionmentioning

confidence: 99%

Effects of Aspirin on Endothelial Function and Hypertension

2016

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Purpose of reviewEndothelial dysfunction is intimately related to the development of various cardiovascular diseases, including hypertension, and is often used as a target for pharmacological treatment. The scope of this review is to assess effects of aspirin on endothelial function and their clinical implication in arterial hypertension.Recent findingsEmerging data indicate the role of platelets in the development of vascular inflammation due to the release of proinflammatory mediators, for example, triggered largely by thromboxane. Vascular inflammation further promotes oxidative stress, diminished synthesis of vasodilators, proaggregatory and procoagulant state. These changes translate into vasoconstriction, impaired circulation and thrombotic complications. Aspirin inhibits thromboxane synthesis, abolishes platelets activation and acetylates enzymes switching them to the synthesis of anti-inflammatory substances.SummaryAspirin pleiotropic effects have not been fully elucidated yet. In secondary prevention studies, the decrease in cardiovascular events with aspirin outweighs bleeding risks, but this is not the case in primary prevention settings. Ongoing trials will provide more evidence on whether to expand the use of aspirin or stay within current recommendations.

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“…In addition, platelets also secrete molecules that have direct antimicrobial properties[111]. For example, in experimental models and human studies of acute infectious settings, platelets circulate with increased surface expression of p-selection.…”

Section: Platelet Secretion In Inflammatory and Infectious Human Disementioning

confidence: 99%

Platelet secretion in inflammatory and infectious diseases

2016

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Platelets are small, anucleate circulating cells that possess a dynamic repertoire of functions spanning the hemostatic, inflammatory, and immune continuum. Once thought to be merely cell fragments with responses limited primarily to acute hemostasis and vascular wall repair, platelets are now increasingly recognized as key sentinels and effector cells regulating host responses to many inflammatory and infectious cues. Platelet granules, including α-granules and dense-granules, store hundreds of factors and secrete these mediators in response to activating signals. The cargo packaged and stored within platelet granules orchestrates communication between platelets and other circulating cells, augments host defense mechanisms to invading pathogens and tumor cells, and – in some settings - drives dysregulated and injurious responses. This focused review will highlight several of the established and emerging mechanisms and roles of platelet secretion in inflammatory and infectious diseases.

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The role of platelets in inflammation

Cited by 380 publications

References 128 publications

Novel Risk Markers and Risk Assessments for Cardiovascular Disease

Novel Risk Markers and Risk Assessments for Cardiovascular Disease

Effects of Aspirin on Endothelial Function and Hypertension

Platelet secretion in inflammatory and infectious diseases

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