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2000

Cardiovascular & Hematological Agents in Medicinal Chemistry (Formerly Current Medicinal Chemistry - Cardiovascular & Hematological Agents) - Current Issue

Volume 23, Issue 2

Volume 23, Issue 2, 2025

    • Novel Pathway and Recent Advances for Targeting Sickle Cell Anemia through Novel Drug Delivery System

      https://doi.org/10.2174/0118715257325911241113075950

      Red 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.

    • Redox-signalling and Redox Biomarkers in Cardiovascular Health and Disease

      https://doi.org/10.2174/0118715257282030240130095754

      Overproduction of reactive nitrogen and oxygen species (RNS and ROS) has been linked to the pathogenesis of diabetes, hypertension, hyperlipidemia, stroke, angina, and other cardiovascular diseases. These species are produced in part by the mitochondrial respiratory chain, NADPH oxidase, and xanthine oxidase. RNS and ROS both contribute to oxidative stress, which is necessary for the development of cardiovascular disorders. In addition to ROS species like hydroxyl ion, hydrogen peroxide, and superoxide anion, RNS species like nitric oxide, peroxynitrous acid, peroxynitrite, and nitrogen dioxide radicals have also been linked to a number of cardiovascular conditions. They promote endothelial dysfunction, vascular inflammation, lipid peroxidation, and oxidative damage, all of which contribute to the development of cardiovascular pathologies. It's crucial to understand the mechanisms that result in the production of RNS and ROS in order to identify potential therapeutic targets. Redox biomarkers serve as indicators of oxidative stress, making them crucial tools for diagnosing and predicting cardiovascular states. The advancements in proteomics, metabolomics, genomics, and transcriptomics have made the identification and detection of these small molecules possible. The following redox biomarkers are notable examples: 3-nitrotyrosine, 4-hydroxy-2-nonenal, 8-iso-prostaglandin F2, 8-hydroxy-2-deoxyguanosine, malondialdehyde, Diacron reactive oxygen metabolites, total thiol, and specific microRNAs (. miRNA199, miRNA21, miRNA1254, miRNA1306-5p, miRNA26b-5p, and miRNA660-5p) are examples. Although redox biomarkers have great potential, their clinical applicability faces challenges. Redox biomarkers frequently have a short half-life and exist in small quantities in the blood, making them challenging to identify and measure. The interpretation of biomarker data may also be influenced by confounding factors and the complex interplay of various oxidative stress pathways. Therefore, in-depth validation studies and the development of sensitive and precise detection methods are needed to address these problems. In the search for redox biomarkers, cutting-edge techniques like mass spectrometry, immunoassays, and molecular diagnostics are applied. New platforms and technologies have made it possible to accurately detect and monitor redox biomarkers, which facilitates their use in clinical settings. Our expanding knowledge of RNS and ROS involvement in cardiovascular disorders has made it possible to develop redox biomarkers as diagnostic and prognostic tools. Overcoming the challenges associated with their utility and utilizing advanced detection techniques, which will improve their clinical applicability, will ultimately benefit the management and treatment of cardiovascular conditions.

    • Factor Xa Inhibitors and Low Molecular Weight Heparins in Perioperative Surgical Thromboprophylaxis: A Network Meta-analysis

      https://doi.org/10.2174/0118715257331706240919172310
      Background

      Venous thromboembolism (VTE) prophylaxis is crucial for reducing the risk of deep vein thrombosis (DVT) and pulmonary embolism (PE). This network meta-analysis was carried out to determine the most effective intervention among selective Xa inhibitors and low molecular weight heparins (LMWHs) for perioperative surgical thromboprophylaxis in major abdominal, pelvic, lumbar spine, and lower limb surgeries.

      Methods

      A systematic literature search was conducted for randomized controlled trials (RCTs) comparing selective factor Xa inhibitors, LMWHs, and placebo as thromboprophylaxis agents in major abdominal, pelvic, lumbar spine, and lower limb surgeries. A Bayesian network meta-analysis was performed to compare all interventions for the risk of developing DVT, VTE, major VTE, total bleeding, and major bleeding. The surface under the cumulative ranking curves was used to rank all interventions.

      Results

      Of 1788 retrieved references, 42 RCTs comparing 11 anticoagulants were included. As compared to enoxaparin, the risk of DVT was significantly reduced in patients treated with fondaparinux [RR: 0.53 (95% CrI: 0.31, 0.93)] and rivaroxaban [RR: 0.42 (95% CrI: 0.27, 0.64)]; VTE in patients treated with bemiparin [RR: 0.09 (95% CrI: 0, 0.7)], edoxaban [RR: 0.43 (95% CrI: 0.18, 0.96)], fondaparinux [RR: 0.55 (95% CrI: 0.34, 0.91)] and rivaroxaban [RR: 0.56 (95% CrI: 0.34, 0.85)]; major VTE in patients treated with rivaroxaban [RR: 0.26 (95% CrI: 0.11, 0.6)]. According to the surface under the cumulative ranking curves (SUCRA) value, fondaparinux and bemiparin increase the risk of serious bleeding more than other factor Xa inhibitors and LMWHs.

      Conclusion

      Rivaroxaban, fondaparinux, edoxaban, and bemiparin are superior perioperative thromboprophylaxis agents than enoxaparin in major surgeries. Fondaparinux and bemiparin have shown the highest risk of major bleeding compared to other factor Xa inhibitors and LMWHs.

    • The Effect of CD31 on Coronary Collateral Development

      https://doi.org/10.2174/0118715257300068240819071920
      Background

      Coronary 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.

      Objectives

      In 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.

      Results

      CD31 levels were significantly higher in the group with coronary artery disease compared to the control group ( <0.001). In addition, CD31 levels in the subgroup with good collateral were significantly higher than in the group with weak collateral ( <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.

      Conclusion

      CD31, a marker of angiogenesis, may be involved in coronary collateral development.

    • Anti-thrombotic Mechanisms of Echinochrome A on Arterial Thrombosis in Rats: , and Studies

      https://doi.org/10.2174/0118715257332064241104114546
      Background

      Arterial 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.

      Objectives

      The current study aims to investigate the effect and mechanism of Ech-A to inhibit thrombus formation induced by ferric chloride in rats.

      Methods

      Twenty-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.

      Results

      The 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.

      Conclusion

      The 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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