Update on pathological platelet activation in coronary thrombosis.
Edoardo EliaFabrizio MontecuccoPiero PortincasaAmir Hossein SahebkarHamid MollazadehFederico CarbonePublished in: Journal of cellular physiology (2018)
Although coronary thrombosis (CT) is integral to cardiovascular outcomes, the underlying pathophysiological mechanisms remain unclear. CT may occur in case of atherosclerotic plaque erosion/rupture, or even after stenting implantation. Platelets (PLT) activation is the keystone of atherothrombosis and depends on many dysregulated elements, including endothelial dysfunction, oxidized lipoproteins, and immune response. Besides the classical view of PLT as an effector of hemostatic response, a new repertoire of PLT activities is emerging. PLT lipidome oxidation is a self-maintaining process which promotes PLT reactivity, coagulation cascade, and inflammatory cell activation. PLT-innate immune cell interaction is also sustained by neutrophil extracellular traps and NLRP3 inflammasome pathways. Other noteworthy emerging mechanisms are implicated in the crosstalk between PLT and surrounding cells. Especially, microvesicles (MVs) released from PLT may extend their signaling network far beyond the classical cell-cell interactions. Moreover, the recognition of noncoding RNA in PLT MVs introduce another layer of complexity in terms of intercellular signaling by a direct regulation of messenger RNA profile and gene expression in the recipient cells. The aim of this narrative review is to update the recent advance in CT and intracoronary stent thrombosis, including causal factors and potential translation of experimental evidence into the clinical setting.
Keyphrases
- immune response
- gene expression
- single cell
- induced apoptosis
- nlrp inflammasome
- pulmonary embolism
- computed tomography
- coronary artery disease
- image quality
- coronary artery
- cell therapy
- dual energy
- cell cycle arrest
- oxidative stress
- magnetic resonance imaging
- dna methylation
- dendritic cells
- heart failure
- atrial fibrillation
- cell death
- magnetic resonance
- stem cells
- positron emission tomography
- nitric oxide
- mesenchymal stem cells
- hydrogen peroxide
- signaling pathway
- risk assessment
- st elevation myocardial infarction