Hydrogen Sulfide and Platelets: A Possible Role in Thrombosis

Abstract

Platelets are circulating blood elements with key roles in haemostasis and thrombosis. Platelets are activated by a range of stimuli including exposed subendothelial components. Haemostasis also depends upon the effects of inhibitory substances, including the gasotransmitter nitric oxide whose effects on platelets are well documented. Evidence is also emerging to suggest that H2S is generated enzymatically by platelets and can impact their function. Exposure of platelets to H2S from slow-release compounds inhibits aggregation and exerted anti-thrombotic effects in vivo. The mechanisms by which H2S impacts platelet function and the importance of interactions between H2S and other gasotransmitters remain unclear. H2S is therefore emerging as a potentially important regulator of platelet activation and thrombosis. Further study is required to evaluate its importance as a regulator of platelet physiology and associated pathological conditions such as myocardial infarction and stroke.

Role of hydrogen sulfide in endothelial dysfunction: Pathophysiology and therapeutic approaches

“…Many studies demonstrated that H 2 S behaves as a vasculoprotective gasotransmitter by modulating different cellular pathways and interfering with a variety of vascular diseases. Indeed, H 2 S inhibits atherogenic modification of low-density lipoproteins (LDL) [11] , prevents monocytes adhesion due to ECs activation [12] , clearly promotes vasorelaxing responses [13] , decreases intimal hyperplasia by inhibiting vascular smooth muscle cells (VSMC) migration and proliferation [14] , limits vascular calcification [15] , thrombogenesis and platelet aggregation [16] , inhibits macrophage foam cell formation and degranulation [17] , limits inflammatory responses and reduces plasma homocysteine (Hcy) levels in experimental animals [18] .…”

Inflammatory Mediators of Endothelial Dysfunction

“…H2S also inhibits vascular calcification, thrombogenesis platelet aggregation, and macrophage foam cell formation and degranulation. Moreover, it could reduce inflammatory responses and the plasma levels of homocysteine (Hcy) in vivo [ 106 , 107 , 108 , 109 , 110 , 111 , 112 ]. In specific cases, CSE deletion from the endothelium was associated with endothelial inflammation and atherosclerosis, which was then reversed by polysulfide donors [ 113 , 114 ].…”

COVID-19: A Redox Disease—What a Stress Pandemic Can Teach Us About Resilience and What We May Learn from the Reactive Species Interactome About Its Treatment

“…Blood cells use the RSI to adjust their function according to environmental cues (including shear stress and redox status). ROS are, in fact, also important intraplatelet signalling entities, with NOX2 playing a key role (436,466); in conjunction with NO and H 2 S they regulate platelet aggregation, adhesion and platelet/leukocyte interactions (106,335). RAS-mediated alterations in RSI signalling may be linked to COVID-associated coagulopathy, inflammation and immune hyperactivity by affecting the clotting process, endothelial leukocyte adhesion/rolling, macrophage polarization, T-cell and erythrocyte function.…”