P5147Direct factor Xa inhibition prevents cardiac remodeling induced by intermittent hypoxia through PAR-1/2 dual signaling pathway

Shimada, M.; Imano, Hideki; Fujiwara, Ayumi; Hashimoto, Takashi; Kato, Ryuichi; Ijiri, Yoshio; Izumi, Yasukatsu; Yoshiyama, Minoru; Hayashi, Toshio

doi:10.1093/eurheartj/ehx493.p5147

Cited by 1 publication

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“…However, and although of a different clinical context pertaining to hypoxic effects on ventricular remodeling, another study showed the exact opposite, as endothelial cells from hypoxic mice treated with a PAR-1 antagonist demonstrates downregulated NF-κB levels. The same study showed similar results with rivaroxaban, an anticoagulant drug which functions by directly targeting the clotting factor Xa [143]. In another study, rivaroxaban was demonstrated to attenuate deep venous thrombosis in a rat model by targeting NF-κB signaling pathway in endothelial cells, more specifically downregulating IκB levels as well as NF-κB levels and activity and thereby performing anti-inflammatory and pro-fibrinolytic functions [144].…”

Section: Natural/pharmacological Compounds and Nf-κbmentioning

confidence: 73%

Role of NF-κB in Platelet Function

Kojok

El-Kadiry

Merhi

2019

IJMS

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Platelets are megakaryocyte-derived fragments lacking nuclei and prepped to maintain primary hemostasis by initiating blood clots on injured vascular endothelia. Pathologically, platelets undergo the same physiological processes of activation, secretion, and aggregation yet with such pronouncedness that they orchestrate and make headway the progression of atherothrombotic diseases not only through clot formation but also via forcing a pro-inflammatory state. Indeed, nuclear factor-κB (NF-κB) is largely implicated in atherosclerosis and its pathological complication in atherothrombotic diseases due to its transcriptional role in maintaining pro-survival and pro-inflammatory states in vascular and blood cells. On the other hand, we know little on the functions of platelet NF-κB, which seems to function in other non-genomic ways to modulate atherothrombosis. Therein, this review will resemble a rich portfolio for NF-κB in platelets, specifically showing its implications at the levels of platelet survival and function. We will also share the knowledge thus far on the effects of active ingredients on NF-κB in general, as an extrapolative method to highlight the potential therapeutic targeting of NF-κB in coronary diseases. Finally, we will unzip a new horizon on a possible extra-platelet role of platelet NF-κB, which will better expand our knowledge on the etiology and pathophysiology of atherothrombosis.

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Section: Natural/pharmacological Compounds and Nf-κbmentioning

confidence: 73%