Some vitamins have beneficial effects on cardiovascular diseases, normalizing platelet function and preventing their excess activation. Anti-platelet vitamins can act directly through inhibitory biochemical pathways in platelets or indirectly by preventing damage to the endothelium or low-density lipoprotein from oxidation. As a rule, each vitamin alone is a weak inhibitor of platelet aggregation. However, in combination, they may act synergistically or enhance the effects of endogenous anti-platelet compounds, such as prostacyclin or nitric oxide, and appear to have a sufficient anti-thrombotic effect. This review will focus on vitamins, which inhibit platelet activation and the mechanisms of their action. The relationship between the vitamins that inhibit platelet aggregation and vascular diseases is examined.
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http://dx.doi.org/10.1080/09537104.2019.1652262 | DOI Listing |
BMC Pregnancy Childbirth
January 2025
Department of Intensive Care Medicine, Army Medical Center of PLA, No. 10 Changjiang Road, Yuzhong District, Chongqing, 400010, People's Republic of China.
Background: Pregnancy-associated atypical hemolytic uremic syndrome (aHUS) is a form of thrombotic microangiopathy (TMA) caused by uncontrolled activation of the complement system during pregnancy or the postpartum period. In the intensive care unit, aHUS must be differentiated from sepsis-related multiple organ dysfunction, thrombotic thrombocytopenic purpura (TTP), hemolysis, elevated liver enzymes, and low platelet (HELLP) syndrome. Early recognition of aHUS is critical for effective treatment and improved prognosis.
View Article and Find Full Text PDFSemin Thromb Hemost
January 2025
of Medicine, Universita degli Studi di Padova Scuola di Medicina e Chirurgia, Padova, Italy.
Anti-platelet factor 4 (PF4) antibody-mediated disorders are a heterogenous group of diseases characterized by the presence of highly pathogenic immunoglobulins G directed against PF4 and/or PF4/heparin complexes. These antibodies are able to activate platelets, neutrophils and monocytes, thus resulting in thrombocytopenia and a hypercoagulable state. Five different forms of anti-PF4 antibody-mediated disorders have been identified: i) classic heparin-induced thrombocytopenia (cHIT) mediated by heparin and certain polyanionic drugs; ii) autoimmune HIT (aHIT) characterized by the presence of anti-PFA/polyanion antibodies that can strongly activate platelets even in the absence of heparin; iii) spontaneous HIT (spHIT) characterized by thrombocytopenia and thrombosis without proximate exposure to heparin, with two subtypes: (a) post-total knee arthroplasty, and cardiac surgery using cardiopulmonary bypass or extracorporeal membrane oxygenation, and (b) post-infections; iv) vaccine-induced immune thrombotic thrombocytopenia (VITT) characterized by thrombocytopenia, arterial and venous thrombosis, or secondary hemorrhage after receiving adenoviral vector vaccines for COVID-19; v) VITT-like disorders triggered by adenoviral infections.
View Article and Find Full Text PDFJ Ethnopharmacol
January 2025
State Key Laboratory of Medicinal Chemical Biology, College of Pharmacy and Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Tianjin, China.
Biomarkers
January 2025
PMI R&D, Philip Morris Products S.A., Neuchâtel, Switzerland.
Background: Growing evidence indicates that noncombustible products could be a tobacco harm reduction tool for smokers who do not quit. The Tobacco Heating System (THS) emits substantially lower levels of harmful cigarette smoke constituents, and previous randomized clinical studies showed improved levels of biomarkers of potential harm (BoPH) linked to smoking-related disease.
Methods: In this cross-sectional study of healthy participants (n = 982) who (i) smoked cigarettes, (ii) had voluntarily switched from smoking to THS use, or (iii) formerly smoked, blood and urine samples were assayed for nine BoPH.
Platelets
December 2025
Cyrus Tang Medical Institute, The Fourth Affiliated Hospital of Soochow University, Collaborative Innovation Center of Hematology, State Key Laboratory of Radiation Medicine and Prevention, Soochow University, Suzhou, China.
Recent studies have shown that anti-ERp5 antibodies inhibit platelet activation and thrombus formation; Moreover, ERp5-deficient platelets exhibit enhanced platelet reactivity via regulation of endoplasmic reticulum (ER) stress. In this study, we used a new ERp5-knockout mouse model as well as recombinant ERp5 (rERp5) protein, to examine the role of ERp5 in platelet function and thrombosis. Although platelet-specific ERp5-deficient mice had decreased platelet count, the mice had shortened tail-bleeding times and enhanced platelet accumulation in FeCl-induced mesenteric artery injury, compared with wild-type mice.
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