scispace - formally typeset
Search or ask a question

Why platelet proteomics is importaint in understaing molecular mechanisam? 


Best insight from top research papers

Platelet proteomics is important in understanding molecular mechanisms because it allows for the identification and quantification of platelet proteins, as well as the detection of post-translational modifications . It provides insights into the complex network of signaling pathways involved in platelet function and regulation . By studying platelet proteomics, researchers can gain a better understanding of platelet biology and its role in various physiological and pathophysiological processes, including cardiovascular diseases, thrombosis, and cancer . Proteomic techniques also help in the discovery of new biomarkers for early diagnosis and potential drug targets . Additionally, platelet proteomics can contribute to the development of personalized medicine and improve patient care by providing valuable information about platelet activity during drug treatments . Overall, platelet proteomics plays a crucial role in advancing our knowledge of platelet function and its implications in health and disease.

Answers from top 5 papers

More filters
Papers (5)Insight
Platelet proteomics is important in understanding molecular mechanisms because it allows for the identification of proteins and interactions involved in platelet biology, which can provide valuable information for both basic science and clinical applications.
Open accessJournal ArticleDOI
Paula Vélez, Ángel García 
22 Citations
Platelet proteomics is important in understanding molecular mechanisms because it allows for the identification of platelet molecular and functional changes in normal and pathological states, providing insights into platelet biology and potential biomarkers and drug targets for cardiovascular diseases.
Platelet proteomics is important in understanding molecular mechanisms because it helps identify and quantify new platelet proteins, reveal post-translational modifications, and provide molecular biomarkers for platelet dysfunctions and genetic aberrations.
Platelet proteomics is important in understanding molecular mechanisms because it enables a holistic understanding of platelet biology by capturing dysregulated molecular processes and integrating them into a broader network of biological systems.
Platelet proteomics is important in understanding molecular mechanisms because it allows for the identification and quantification of proteins, unraveling post-translational modifications, and monitoring platelet activity during drug treatments.

See what other people are reading

How to numerically simulate electrolysis around catheter in blood?
5 answers
To numerically simulate electrolysis around a catheter in blood, one can utilize computational models that consider various factors. Models integrating blood dynamics with the Navier-Stokes equations and substance dispersion through advection diffusion equations can simulate the physical processes during catheter injection. Additionally, incorporating a dynamic computational fluid program can help simulate blood flow within central venous catheters, assessing factors like shear stress, velocity, and pressure, especially when catheters are obstructed. Furthermore, adapting finite element modeling programs can provide accurate solutions for laminar blood flow around intra-arterial catheters, aiding in predicting thrombus activation sites and deposition through analysis of velocity, pressure fields, shear rates, and particle paths. These approaches can collectively contribute to a comprehensive numerical simulation of electrolysis around catheters in blood, considering both fluid dynamics and catheter design aspects.
Why crude aspirin insoluble?
5 answers
Crude aspirin is insoluble due to its poor aqueous solubility. This limitation affects its dissolution properties in biological systems, impacting its bioavailability. Various techniques have been explored to enhance the solubility of aspirin, such as cocrystallization with coformers like benzoic acid, and production of micronized aspirin and aspirin/polyethylene glycol 4000 composites. Additionally, forming complexes of aspirin with phosphoric acid has been studied to improve its solubility and bioavailability. These studies highlight the importance of addressing the solubility issues of aspirin through different methods to enhance its therapeutic effectiveness.
Ticagrelor inhibitory effect on activation of STAT3 signaling pathway?
5 answers
Ticagrelor has been extensively studied for its pharmacological effects beyond platelet inhibition. While it inhibits various pathways like NLRP3 inflammasome activation, GSK-3β/caspase-1/GSDMD activation, and platelet-neutrophil interactions leading to NET formation, there is no direct evidence in the provided contexts regarding its inhibitory effect on the STAT3 signaling pathway. The research primarily focuses on ticagrelor's impact on inflammation, pyroptosis, and platelet-related processes. Therefore, based on the available data, there is no indication that ticagrelor directly inhibits the activation of the STAT3 signaling pathway.
Ticagrelor inhibitory effect on activation of NF-kB signaling pathway?
5 answers
Ticagrelor exhibits inhibitory effects on the activation of the NF-κB signaling pathway. It prevents the degradation of IKBα, phosphorylation of p65, and the translocation of p65 into the nucleus, thereby reducing the production of inflammatory factors like TNFα, IL-1, IL-8, IL-6, and IL-2. Ticagrelor also downregulates NF-κB and galectin-3 expressions, along with IL-6 and TNF-α levels, in ischemic conditions. Moreover, ticagrelor inhibits the NLRP3 inflammasome activation independent of its classic P2Y12 inhibitory effect, showing promise in mitigating systemic inflammation. These findings collectively suggest that ticagrelor's modulation of the NF-κB pathway contributes to its anti-inflammatory properties, highlighting its potential therapeutic role in conditions involving NF-κB-mediated inflammation.
Characterization of E.coli in lungs of rabbit?
5 answers
E. coli has been implicated in lung-related pathologies in rabbits. Studies have shown that intratracheal instillation of E. coli can induce acute lung injury (ALI) in rabbits, leading to significant changes in various lung parameters. Additionally, E. coli lipopolysaccharide (LPS) infusion in rabbits has been linked to alterations in leukocyte counts, blood gases, and pulmonary vascular function, highlighting the impact of E. coli on lung physiology. Furthermore, the pathogenicity of extraintestinal pathogenic E. coli (ExPEC) in dog and cat lung samples has been investigated, revealing a correlation between virulence factors like P fimbriae, hemolysin D, and cytotoxic necrotizing factor 1 with bacterial pneumonia-induced mortality, particularly in phylogroups B1 and B2. These findings collectively emphasize the significance of understanding E. coli's role in lung infections and associated pathogenic mechanisms in rabbits.
What is the role of neutrophil-monocyte aggregates?
5 answers
Neutrophil-monocyte aggregates play a crucial role in various pathological conditions. These aggregates are influenced by inflammation and can contribute to exacerbating inflammatory responses in diseases like atherosclerosis and lupus. In atherosclerosis, monocyte-platelet aggregates are associated with disease progression, especially during acute events like myocardial infarction. In autoimmune diseases like lupus, neutrophils interact with immune complexes, leading to the activation of immune cells and tissue damage. Furthermore, neutrophils in Papillon-Lefevre syndrome lack the ability to form neutrophil extracellular traps (NETs) and associated aggregates, which results in nonresolving periodontitis due to the absence of a negative feedback mechanism for inflammation. Overall, neutrophil-monocyte aggregates are pivotal in linking inflammatory and immune responses in various diseases.
How does the interaction between platelets and neutrophils contribute to the development of atherosclerosis?
5 answers
The interaction between platelets and neutrophils plays a crucial role in the development of atherosclerosis. Neutrophils, traditionally known for their role in infection and inflammation, have been found to accumulate within atherosclerotic plaques, promoting a "second wave" of macrophage migration and accumulation. Platelet-neutrophil interaction activates inflammatory pathways, such as Mrp8/14 and TLR4, leading to the release of inflammatory mediators and inhibition of neutrophil apoptosis, ultimately exacerbating atherosclerosis progression. Additionally, platelets contribute to the inflammatory environment by interacting with various inflammatory cells, secreting cytokines, and inducing the activation of other platelets and endothelial cells, further promoting atherosclerosis development. This intricate interplay between platelets and neutrophils underscores their significant contribution to the pathogenesis of atherosclerosis.
Can platelet activation be disrupted by lipoprotein(a)?
5 answers
Platelet activation can indeed be disrupted by lipoprotein(a) (Lp(a). Research indicates that Lp(a) interacts with platelets, affecting their function. Specifically, Lp(a) inhibits platelet activation induced by platelet activating factor (PAF) in a dose-dependent manner, as well as aggregation triggered by other agonists like ADP or Calcium ionophore A23187. Moreover, Lp(a) reduces the surface expression of platelet integrin-receptor αIIbβ3 and inhibits fibrinogen binding to activated platelets, further disrupting platelet activation. However, it's important to note that conflicting findings exist, with some studies suggesting no significant association between Lp(a) levels and platelet reactivity. Overall, Lp(a) can interfere with platelet activation, potentially impacting thrombotic processes.
What is the influence of gotu cola on the kidneys?
5 answers
Gotu cola, also known as Centella asiatica, is not directly addressed in the provided contexts. However, studies have explored the impact of different fluids and substances on kidney health. Cola beverages have been associated with increased risk factors for kidney stones, while cocaine abuse has been linked to acute kidney injury and chronic kidney disease. The consumption of cola beverages has been shown to lead to unfavorable changes in risk factors associated with calcium oxalate stone formation, suggesting that patients may need to avoid this drink to maintain kidney health. In contrast, fluids containing citric acid, like Fresca, may help attenuate stone activity. Overall, while the influence of gotu cola specifically is not discussed, these studies highlight the importance of fluid choices and substance abuse in kidney health.
What was the pipeline that led to discovery of lapatinib?
5 answers
The discovery of lapatinib, a dual EGFR and ERBB-2 tyrosine kinase inhibitor, involved a carefully designed biological evaluation cascade coupled with multidimensional data analysis. Lapatinib was initially identified as a multitargeted inhibitor of phosphoprotein signaling in Trypanosoma brucei, despite lacking EGFR-like tyrosine kinases, through proteome-wide phosphopeptide analysis and affinity chromatography studies. Lapatinib's efficacy against HER2-amplified breast cancer was further explored, showing activity in trastuzumab-refractory cases and in combination with letrozole for ER-positive, HER2-positive breast cancer. However, lapatinib exhibited limited activity against the xenografts of the Pediatric Preclinical Testing Program (PPTP) in vivo panel, suggesting differences in therapeutic targets between adult and pediatric cancers.
What is the molecular mechanism behind platelet aggregation due to ibuprofen?
5 answers
Platelet aggregation induced by ibuprofen involves complex molecular mechanisms. Studies show that ibuprofen can interact synergistically with platelet mediators like arachidonic acid (AA) or 5-hydroxytryptamine (5-HT), leading to increased aggregation. The synergistic effect of AA with 5-HT or adenosine diphosphate (ADP) on platelets is inhibited by cyclooxygenase (COX) inhibitors and other specific inhibitors, highlighting the involvement of COX/thromboxane A2, receptor-operated Ca(2+) channels, Gq/PLC, and MAPK signaling pathways in this process. Additionally, ibuprofen derivatives have been synthesized and shown to protect platelets by mitigating oxidative stress-induced platelet apoptosis and inhibiting platelet aggregation, suggesting a potential therapeutic role in conditions associated with platelet activation and thrombocytopenia.