Platelet Activation Polymorphisms in Ischemia

Haybar, Habib; Khodadi, Elahe; Zibara, Kazem; Saki, Najmaldin

doi:10.2174/1871529x18666180326121239

Cited by 15 publications

(13 citation statements)

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“…In this regard, an association between rs1131882, rs4311994 and rs3779647 and increased platelet activity in diabetic patients on aspirin therapy has already been reported (Postula et al, 2011;Postula et al, 2013). Studies also indicated that the presence of genetic variations in the COX-2 gene such as rs5275 boosts COX-2 expression and therefore aid in reducing the risk of myocardial infarction and ischemia; cardiac conditions in which platelet activation makes an important contribution (Haybar et al, 2018). rs4251961 was associated with higher expression of fibrinogen that plays a key role in hemostasis, and thus participates in the prevention of bleeding (Wassel et al, 2011).…”

Section: Discussionmentioning

confidence: 95%

Influence of Polymorphisms Involved in Platelet Activation and Inflammatory Response on Aspirin-Related Upper Gastrointestinal Bleeding: A Case-Control Study

et al. 2020

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Background: Despite the wide benefits of aspirin and its cost-effectiveness, aspirin prescriptions have been reduced due to idiosyncratic responses in susceptible individuals. Low-dose aspirin and single-nucleotide polymorphisms (SNPs) are independently associated with increased risk of gastrointestinal hemorrhage; however, to-date, no studies investigated the SNP-aspirin interaction effect on upper gastrointestinal hemorrhage (UGIH). Therefore, we aimed to evaluate the role of 25 SNPs in multiple genes involved in platelet activation, angiogenesis and inflammatory response in aspirin-related UGIH. Methods: A multicenter, full case-control study was conducted in patients exposed and unexposed to aspirin. Three hundred twenty-six cases diagnosed with UGIH were matched with 748 controls (1:3) by age, gender, health center, and recruitment date. Only adults of European origin were included. Participants were stratified by aspirin exposure and genotype [(Aspirin (−) , wild-type), (Aspirin (+) , wild-type), (Aspirin (+) , genetic variation), (Aspirin (−) , genetic variation)]. For each SNP, the Odds Ratio of UGIH and their 95% confidence intervals were estimated in each subgroup by using the generalized linear mixed models for dependent binomial variables. SNP-aspirin interaction effect was estimated through Relative Excess Risk due to Interaction (RERI) measures.

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Section: Discussionmentioning

confidence: 95%

Influence of Polymorphisms Involved in Platelet Activation and Inflammatory Response on Aspirin-Related Upper Gastrointestinal Bleeding: A Case-Control Study

et al. 2020

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“…In conclusion, although SerpinB2 has classically been associated with inhibition of uPA-mediated fibrinolysis, we illustrate herein that SerpinB2 (at least in mice) has an unexpected plateletassociated activity in the regulation clot formation. Further research is required to ascertain how relevant this new role for SerpinB2 might be in human diseases [6,9,[41][42][43][44][45].…”

Section: Discussionmentioning

confidence: 99%

SerpinB2 deficiency in mice reduces bleeding times via dysregulated platelet activation

Schroder

Gardner

et al. 2018

Platelets

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SerpinB2, also known as plasminogen activation inhibitor type 2 (PAI-2), is classically viewed as an inhibitor of fibrinolysis. However, we show herein a distinct, hitherto unrecognized role for SerpinB2 in hemostasis. Mice deficient in SerpinB2 expression and mice with an active site mutation in SerpinB2, both showed significant reductions in tail bleeding times. This hemostatic phenotype was associated with platelets, with SerpinB2 and SerpinB2-urokinase complexes clearly present in platelet fractions, and immunohistochemistry of blood clots suggesting SerpinB2 is associated with platelet aggregates. Thromboelastography illustrated faster onset of clot formation in blood from SerpinB2 deficient mice, whereas clotting of platelet-free plasma was unaffected. The results appear consistent with the low circulating SerpinB2 levels and hypercoagulation seen during pre-eclampsia; however, SerpinB2 was not detected in human platelets.

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“…The inhibition of a number of molecules protecting the cardiac tissue after injury is regulated by different signaling pathways (Deb, ; Haybar, Khodadi, Shahjahani, & Saki, ; Haybar, Khodadi, Zibara, & Saki, ). HSF1 is a molecule expressed after damage to cardiomyocytes or other cardiac cell populations, which prevents cardiac dysfunction and leads to homeostasis through HSPs expression (Krishnamurthy, Vedam, Kanagasabai, Druhan, & Ilangovan, ; Peng et al, ).…”

Section: Discussion and Future Perspectivementioning

confidence: 99%

Protective role of heat shock transcription factor 1 in heart failure: A diagnostic approach

Haybar

Shahrabi

Rezaeeyan

et al. 2018

Journal Cellular Physiology

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Objective Nonexpression or expression inhibition of protective factors has been determined in the occurrence of heart failure (HF). Heat shock transcription factor 1 (HSF1) is among such factors, which reduces the incidence of HF by controlling cardiac hypertrophy and fibrosis. In this study, molecular mechanisms for nonexpression of HSF1 in HF patients have been investigated. Materials and methods This review paper is based on the material obtained via PubMed search of 1996–2018. The key search terms were "heart failure," "heat shock transcription factor 1," "hypertrophy", "fibrosis," and "apoptosis." Results Although factors such as janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) and heat shock proteins (HSPs) may respectively increase and decrease susceptibility to HF, in some circumstances, these factors may unexpectedly prevent HF progression. Conclusion Finally, identification of molecular pathways expressed by various factors could be used to design appropriate treatments or to employ strategies inducing the expression of HSF1 to prevent HF.

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Platelet Activation Polymorphisms in Ischemia

Abstract: In this review, we have evaluated the role of polymorphisms involved in platelet activation and development of ischemia.

Cited by 15 publications

References 0 publications

Influence of Polymorphisms Involved in Platelet Activation and Inflammatory Response on Aspirin-Related Upper Gastrointestinal Bleeding: A Case-Control Study

Influence of Polymorphisms Involved in Platelet Activation and Inflammatory Response on Aspirin-Related Upper Gastrointestinal Bleeding: A Case-Control Study

SerpinB2 deficiency in mice reduces bleeding times via dysregulated platelet activation

Protective role of heat shock transcription factor 1 in heart failure: A diagnostic approach

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