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Cardiovascular & Hematological Agents in Medicinal Chemistry (Formerly Current Medicinal Chemistry - Cardiovascular & Hematological Agents) - Online First
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Emerging Biomarkers for Assessing Thrombotic Risk in Patients Receiving Direct Oral Anticoagulants (DOACs)
Authors: Ashmi Sabana M. and Alwin Simon M.Available online: 16 December 2024More LessDirect Oral Anticoagulants (DOACs) have transformed the management of thrombotic disorders, offering a more convenient and effective alternative to traditional vitamin K antagonists (VKAs). However, assessing thrombotic risk in patients treated with DOACS remains crucial due to the potential for recurrent events. Current clinical risk scores have limitations in predicting and monitoring venous thromboembolism (VTE) risk in specific DOAC populations. Several emerging biomarkers show promise in assessing thrombotic risk in patients treated with DOACS. Genetic factors like VKORC1 and CYP2C9 variants are well-established determinants of warfarin response, but the genetic landscape for DOAC outcomes appears more complex. Rare variants and polygenic approaches may play a role in personalizing anticoagulation therapy. Elevated factor VIII levels are associated with increased VTE recurrence risk after anticoagulation withdrawal in cancer-associated thrombosis (CAT) patients. In contrast, the circulating tissue factor is not useful for predicting VTE in this setting. Soluble P-selectin has emerged as a good marker of VTE recurrence, and its inclusion in the Vienna CATS risk model improves VTE prediction in cancer patients. While these biomarkers hold promise, larger studies are needed to validate their utility and establish standardized assays. Caution is warranted in patients at high bleeding risk. Integrating clinical factors, genetics, and circulating biomarkers will likely optimize thrombotic risk assessment in patients treated with DOACS. Continued research is crucial to develop personalized anticoagulation strategies to balance thrombosis and bleeding risks.
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Novel Pathway and Recent Advances for Targeting Sickle Cell Anemia through Novel Drug Delivery System
Authors: Savita Chouhan, Ajazuddin and Parag JainAvailable online: 03 December 2024More LessRed blood cells with sickle cell anemia (SCA) have an irregular shape, and it is a genetic blood condition that can cause several problems and shorten life expectancy. Traditional treatments have focused on symptom management, but recent advancements in drug delivery systems offer promising pathways for targeted therapies. This abstract explores novel approaches to combat SCA through innovative drug delivery systems, gene therapy, and new pharmaceutical interventions. One novel pathway for targeting SCA involves utilizing advanced drug delivery systems to enhance the effectiveness of therapeutic agents. Nanotechnology-based delivery systems, such as nanoparticles and liposomes, offer precise drug targeting, controlled release, and improved bioavailability. These systems can encapsulate anti-sickling agents, like hydroxyurea, and enable their specific delivery to affected cells, reducing side effects and enhancing therapeutic outcomes. Additionally, therapy has become a ground-breaking method of treating SCA. CRISPR/Cas9 technology presents a groundbreaking opportunity to correct the genetic mutation responsible for sickle hemoglobin production. By precisely editing the HBB gene, which encodes the abnormal hemoglobin, researchers aim to restore normal hemoglobin expression, potentially offering a curative treatment for SCA. Furthermore, recent advancements in drug development have led to the discovery of promising candidates targeting specific pathways involved in SCA pathophysiology. Experimental drugs, such as voxelotor and crizanlizumab focus on modifying hemoglobin properties or inhibiting cell adhesion, respectively, thereby preventing sickle cell-related complications and reducing vaso-occlusive crisis frequency.
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Anti-thrombotic Mechanisms of Echinochrome A on Arterial Thrombosis in Rats: In-Silico, In-Vitro and In-Vivo Studies
Available online: 12 November 2024More LessBackgroundArterial thrombosis is one of the most significant healthcare concerns in the world. Echinochrome A (Ech-A) is a natural quinone pigment isolated from sea urchins. It has a variety of medicinal values associated with its antioxidant, anticancer, antiviral, anti-diabetic, and cardio-protective activities.
ObjectiveThe current study aims to investigate the effect and mechanism of Ech-A to inhibit thrombus formation induced by ferric chloride in rats.
MethodsTwenty-four rats were assigned into four groups (n= 6); sham and thrombotic model groups were orally administered 2% DMSO, while the other groups were treated with two dosages of Ech-A (1 and 10 mg/kg, body weight). After seven days of administration, all groups were exposed to 50% ferric chloride for 10 min, except the sham group exposure to normal saline.
ResultsThe molecular docking showed the free binding energies of Ech-A and vitamin K (Vit. K) with Vit. K epoxide reductase were -8.5 and -9.8 kcal/mol, which confirm the antithrombotic activity of Ech-A. The oral administration of Ech-A caused a significant increase in partial thromboplastin time, prothrombin time, clotting time, platelet count, fibrinogen levels, factor VIII, glutathione reduced, catalase, nitric oxide, and glutathione S-transferase. While white blood cells count, calcium level, and malondialdehyde concentration significantly decreased. The histological examination revealed a definite improvement in the carotid and cardiac tissues in the Ech-A groups.
ConclusionThe study results showed that Ech-A prevented thrombosis by several mechanisms, including chelating calcium ions, increasing the NO concentration, suppressing oxidative stress, and antagonizing Vit. K.
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Cardio-metabolic Disorders Affected by Genetic Polymorphisms Related to Premature Menopause
Authors: Mohammad Reza Mirinezhad, Hamideh Safarian Bana, Malihe Aghsizadeh, Mohammad Amin Mohammadi, Hamideh Ghazizadeh, Ali Ebrahimi Dabagh, Sayyedeh Helya Mir Nourbakhsh, Hassan Kiani Shahvandi, Alireza ghodsi, Mahdie Aghasizade, Faezeh Taghipour, Elahe Hasanzadeh, Nazanin Sheikh Andalibi, Hamed Khedmatgozar, Gordon A Ferns, Tayebeh Hamzehloei, Alireza Pasdar and Majid Ghayour-MobarhanAvailable online: 05 November 2024More LessBackgroundPremature menopause (PM) is defined as the end of ovulation before the age of 40 years, a condition commonly referred to as primary ovarian insufficiency. It has been shown there is an association between early menopause and a high risk of cardiovascular disease.
AimThis study aimed to evaluate the effect of genetic polymorphisms related to premature menopause on cardio-metabolic disorders
ObjectiveWe aimed to investigate the single nucleotide polymorphisms associated with PM and the risk of cardio-metabolic disorders in the MASHAD cohort study.
MethodsIn this cross-sectional study, a total of 117 women with PM were recruited and compared with 183 healthy women. All participants were assessed for anthropometric indices and genotyped for eight selected polymorphisms within seven different genes.
ResultsA significant difference was observed in physical activity level (PAL) between the groups. Individuals with rs4806660 CC genotype had a 3.63-fold increased risk of metabolic syndrome. Moreover, individuals with a TT genotype of the rs2303369 polymorphism had a 3.11-fold increased risk of obesity.
ConclusionOur findings showed that genetic variations are risk factors related to cardio-metabolic disorders in women with premature menopause.
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The Effect of CD31 on Coronary Collateral Development
Available online: 28 August 2024More LessBackgroundCoronary collaterals are the feeding bridges between the main epicardial arteries, and research has shown that this collateral development plays a crucial role in myocardial performance, especially in patients with coronary artery disease. However, the evolution of these collaterals has not been fully explained.
ObjectiveIn this study, we aimed to reveal the effect of CD31 on coronary collateral development.
Methods: As a result of coronary angiography performed in our clinic, 89 patients with coronary artery disease and 90 patients with normal coronary arteries were included in the study. Collateral development degrees were recorded from the angiographic images of the subjects. CD31 values were compared between the group with coronary artery disease and the control group. In addition, the coronary artery disease group was divided into subgroups according to the collateral development in terms of good collateral development and poor collateral development, and the factors that may affect the collateral development were tried to be determined.
ResultsCD31 levels were significantly higher in the group with coronary artery disease compared to the control group (p <0.001). In addition, CD31 levels in the subgroup with good collateral were significantly higher than in the group with weak collateral (p <0.001). In the correlation analysis, a significant positive correlation was found between serum CD31 level and SYNTAX score, age, glucose, and rentrop grade. Multivariate logistic regression analysis showed CD31 to be an independent predictor of good coronary collateral development.
ConclusionCD31, a marker of angiogenesis, may be involved in coronary collateral development.
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Sodium Butyrate, a Gut Microbiota Derived Metabolite, in Type 2 Diabetes Mellitus and Cardiovascular Disease: A Review
Authors: Zeynab Sarlak, Narges Naderi, Bardia Amidi and Vajihe GhorbanzadehAvailable online: 28 August 2024More LessType 2 diabetes is characterized by elevated blood glucose levels, leading to an increased risk of cardiovascular diseases. Sodium butyrate, the sodium salt of the short-chain fatty acid butyric acid produced by gut microbiota fermentation, has shown promising effects on metabolic diseases, including type 2 diabetes and cardiovascular diseases. Sodium butyrate demonstrates anti-inflammatory, anti-oxidative, and lipid-lowering properties and can improve insulin sensitivity and reduce hepatic steatosis. In this review, we investigate how sodium butyrate influences cardiovascular complications of type 2 diabetes, including atherosclerosis (AS), heart failure (HF), hypertension, and angiogenesis. Moreover, we explore the pathophysiology of cardiovascular disease in type 2 diabetes, focusing on hyperglycemia, oxidative stress, inflammation, and genetic factors playing crucial roles. The review suggests that sodium butyrate can be a potential preventive and therapeutic agent for cardiovascular complications in individuals with type 2 diabetes.
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