Inflammation in venous thromboembolism: Cause or consequence?

Saghazadeh, Amene; Hafizi, Sina; Rezaei, Nima

doi:10.1016/j.intimp.2015.07.044

Cited by 105 publications

(118 citation statements)

References 113 publications

(143 reference statements)

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“…Thus, the formation of thrombus promotes the inflammatory response, which subsequently, stimulates the pro-thrombotic factors. These affirmations are supported by the fact that thrombosis can be prevented by natural anticoagulants, such as protein C and S, antithrombin III, which can also reduce inflammatory activity [1,2,15,[19][20][21].…”

Section: Interaction Between Inflammation and Thrombosismentioning

confidence: 99%

“…An increase in the inflammatory markers, which might reflect an independent inflammatory pro-cess or a subclinical persistent inflammation, may be secondary to other diseases associated with venous thrombosis, such as post-thrombotic syndrome or occult cancer. [15,17,[19][20][21].…”

Section: Interaction Between Inflammation and Thrombosismentioning

confidence: 99%

“…Patients with deep venous thrombosis can benefit from treatment with anti-inflammatory agents or low molecular weight heparins, due to the fact that they hold both anti-inflammatory and anticoagulant properties [19][20][21].…”

Section: Interaction Between Inflammation and Thrombosismentioning

confidence: 99%

“…It was demonstrated that patients with high serum levels of these inflammatory cytokines present a risk 2-3 times higher to develop venous thrombosis [1,17,[19][20][21][22]. Moreover, plasma concentrations of these immune mediators were increased in patients with recurrent venous thrombosis.…”

Section: Il-8 and Il-6mentioning

confidence: 99%

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Involvement of inflammatory markers in pathogenesis of venous thromboembolism

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et al. 2017

Revista Romana De Medicina De Laborator

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Inflammation of the venous wall is involved in thrombogenesis, thrombus resolution, wall remodeling and the post-thrombotic syndrome. Different mechanisms are involved in both arterial and venous thrombosis and patients with atherothrombosis hold a higher risk of venous thrombosis. Although inflammation may represent the connection between arterial and venous thrombosis, it is not yet sure if it is the cause or consequence of venous thrombosis. Consequently, the relationships between inflammation markers as indicators of the inflammatory process and clinical venous thromboembolism need to be investigatd. For example, inflammation mediators such as the pro-inflammatory cytokines interleukin 8 (IL-8), IL-6, monocyte chemotactic protein 1 (MCP-1), C Reactive Protein (CRP), vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), matrix metalloproteinases and tumor necrosis factor alpha (TNF alpha)

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Section: Interaction Between Inflammation and Thrombosismentioning

confidence: 99%

Section: Interaction Between Inflammation and Thrombosismentioning

confidence: 99%

Section: Interaction Between Inflammation and Thrombosismentioning

confidence: 99%

Section: Il-8 and Il-6mentioning

confidence: 99%

See 2 more Smart Citations

Involvement of inflammatory markers in pathogenesis of venous thromboembolism

Cocoi

Pop

Cocoi³

et al. 2017

Revista Romana De Medicina De Laborator

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“…Detachment of thrombi may cause pulmonary embolism and lead to patient mortality (21). Inflammation is a major of the risk factors of DVT (28,29). Various studies have demonstrated that levels of inflammatory cytokines and chemokines are increased in the peripheral blood of patients with DVT.…”

Section: Discussionmentioning

confidence: 99%

Role of microRNA‑26a in the diagnosis of lower extremity deep vein thrombosis in patients with bone trauma

2017

Exp Ther Med

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Abstract. The present study aimed to investigate the role and mechanism of action of microRNA (miR)-26a in deep vein thrombosis (DVT). Peripheral blood was collected from 45 patients with DVT and 40 healthy controls. Levels of miR-26a, chemokine C-C motif ligand (CCL)2 mRNA and CCL7 mRNA were detected using reverse transcription-quantitative polymerase chain reaction and the value of miR-26a in the clinical diagnosis of DVT was assessed using receiver operating characteristic curve analysis. The correlation of miR-26a with CCL2 and CCL7 levels was analyzed using Spearman's rank correlation. In addition, miR-26a and protein kinase C δ (PRKCD) were overexpressed in human umbilical vein endothelial cells (HUVECs) and PRKCD expression was knocked down by small interfering (si)RNA. Western blotting was conducted to detect the expression of PRKCD and p65. Furthermore, a dual-luciferase reporter gene assay was performed. The results of the current study demonstrated that the expression of miR-26a was significantly downregulated in the peripheral blood of patients with DVT compared with healthy controls (P<0.05) and negatively correlated with CCL2 and CCL7 levels (P<0.05). Furthermore, it was demonstrated that miR-26a markedly inhibited the expression of PRKCD, significantly decreased levels of CCL2 and CCL7 mRNA (P<0.05) and inhibited activation of the NF-κB signaling pathway. Overexpression of PRKCD in HUVECs inhibited the effects of miR-26a and markedly upregulated the phosphorylation of p65. The present study indicated that miR-26a directly targets PRKCD mRNA and that miR-26a may be a useful biomarker in the clinical diagnosis of DVT. Thus, the present findings suggest that miR-26a regulates the NF-κB signaling pathway by binding to PRKCD mRNA, inhibits the expression of CCL2 and CCL7 and reduces the risk of DVT.

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