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Cardiovascular & Haematological Disorders - Drug Targets - Volume 25, Issue 3, 2025

Volume 25, Issue 3

Volume 25, Issue 3, 2025

    • IL 6 Cascade in Post COVID Cardiovascular Complications: A Review of Endothelial Injury and Clotting Pathways

      https://doi.org/10.2174/011871529X371965250618060805

      The COVID-19 pandemic has revealed various long-term cardiovascular complications linked to increased inflammatory responses, particularly through Interleukin-6 (IL-6) activity. IL-6 is a major cytokine in the immune system that plays a bimodal role: it supports acute immune defense but contributes to chronic inflammation and tissue damage when dysregulated. High levels of IL-6 during and after COVID-19 are linked with poor outcomes, such as Acute Respiratory Distress Syndrome (ARDS), myocarditis, endothelial dysfunction, and thrombotic events. Chronic IL-6 signaling impairs vascular homeostasis, leading to endothelial dysfunction and increased thrombosis. Viral and cytokine-driven inflammation leads to endothelial damage caused by COVID-19. These include mechanisms that implicate the downregulation of ACE2, oxidative stress, and reduced bioavailability of nitric oxide. All these contribute to arterial stiffness, atherosclerosis, and thrombosis. It is possible to reduce the risk of heart disease by using targeted therapies, such as IL-6 inhibitors, which can help reduce inflammation. Biomarkers of endothelial health and inflammation include EPCs and CECs. Pharmacological strategies, such as RAS inhibitors and statins, may have additive effects on endothelial function, but ACE2 upregulation remains a major question. Rehabilitation and exercise-based approaches are further supportive of vascular recovery. When IL-6 activity stays high after an infection, it causes blood to clot too easily and cause thrombotic problems. This makes patients more likely to experience an ischemic stroke or pulmonary embolism. Anticoagulants and IL-6 inhibitors like tocilizumab reduce these risks. IL-6's long-term effects on the heart need to be studied more, and biomarker screening, lifestyle changes, and personalized therapies must be used to prevent heart disease as much as possible. A holistic management approach that integrates anti-inflammatory and anticoagulation strategies will significantly improve outcomes in survivors of COVID-19.

    • The Impact of Single Nucleotide Polymorphisms and Other Mechanisms on Aspirin Resistance

      https://doi.org/10.2174/011871529X361464250319084053

      Atherosclerosis and ischemic events play a pivotal role in the pathogenesis of several cardiovascular diseases (CVD). The primary aim of preventing recurrent thrombosis in patients who underwent cardiovascular surgery is the antiplatelet agent administration. Nevertheless, despite the aspirin therapy or double (aspirin plus clopidogrel) therapy, the effectiveness of antithrombotic treatment remains controversial. In recent years, we have learned that some percentage of patients still demonstrate no clinical response to aspirin treatment and may experience a vascular complication. This article provides an overview of recent scientific studies that have focused on experimental detection and genotyping of single nucleotide polymorphisms (SNPs) in patients, involving the main therapeutic target genes: cyclooxygenase COX-1 and COX-2, guanylate cyclase GUCY1A3, the glycoprotein complex GPIIb-IIIa, and the platelet receptor protein PEAR1.” The aspirin resistance (AR) ranges considerably from 0% to 66% in patients with ischemic heart disease (IHD) and relatively healthy people (control group). SNP distribution analysis has been proposed to explain the inadequate high platelet reactivity (HPR) among patients with IHD under aspirin treatment. Various SNPs have been proposed to explain the development of CVD and the persistent HPR under aspirin treatment widely used in the prevention of recurrent cardiovascular thrombotic events. Meanwhile, the efficacy of aspirin therapy in secondary thrombosis prevention in patients with IHD is not strongly associated with known SNP. The inconsistent results of different AR clinical trials are likely due to the design of the experiments and methodological and quantitative issues; therefore, careful interpretation of the SNP genotyping results is necessary.

    • The Green Path to Liver Health: Herbal Solutions for Non-alcoholic Steatohepatitis

      https://doi.org/10.2174/011871529X360903250211101856

      Non-alcoholic steatohepatitis (NASH) is a progressive liver disease marked by inflammation and fibrosis, stemming from non-alcoholic fatty liver disease (NAFLD). Despite its rising predominance, current therapeutic medications are limited in efficacy and safety. Recent attention has shifted towards herbal therapies as potential adjuncts or alternatives in NASH management, given their anti-inflammatory, antioxidant, and phospholipid-controlling characteristics. This research study attempted to assess critically existing literature on the efficacy of herbal interventions while managing NASH. The main goal was to assess the possible medicinal advantages of different herbs, highlight their mechanisms of action, and identify gaps in current research to guide future studies. A systematic review of peer-reviewed articles using databases, like PubMed, Scopus, and Google Scholar, was conducted. It included studies that investigated the effects of herbal extracts (., silymarin, curcumin, berberine) on NASH-related outcomes, such as liver function, fibrosis, lipid metabolism, and inflammatory markers. The review identified several herbs with promising therapeutic effects on NASH. Silymarin showed consistent improvements in liver enzymes and fibrosis markers. Curcumin and berberine were effective in reducing inflammation of the liver and oxidative damage. However, the heterogeneity in research designs, dosages, and outcome measures has limited the generalizability of findings. Herbal therapies hold potential as complementary treatments for NASH, with evidence supporting their role in improving liver function and reducing inflammation. To prove their safety and effectiveness, however, greater sample numbers and longer follow-up times are required in standardised clinical studies.

    • Cardiopulmonary and Urine Electrolyte Changes in Healthy Males Exposed to Two Distinct Anaerobic Exercises

      https://doi.org/10.2174/011871529X369260250512024353
      Background

      Anaerobic exercise, characterized by short bursts of high-intensity activity such as weightlifting, sprinting, and high-intensity interval training (HIIT), has been documented to influence the body physiology.

      Objectives

      The study investigated the acute impact of weightlifting and rope jumping exercise sessions on blood pressure, pulse rate, blood glucose, body temperature, pulmonary indices, and urine creatinine and electrolyte levels in healthy male subjects.

      Methods

      Twenty participants, aged 18-25, were randomly assigned to the control group (n=10) and the exercise group (n=10). The control group watched exercise videos of weightlifting and rope jumping, respectively. The anaerobic exercise group performed weightlifting and rope jumping exercise sessions, respectively. Before the commencement of the experiment, the participants were given a 15-minute rest, and their blood pressure, body temperature, and blood glucose were measured. Then they were given 600 mL of water and 15 g of glucose for hydration and energy. After 45 minutes, their cardiovascular indices, blood glucose, body temperature, pulmonary indices, and urine sample for assessment of urine electrolyte and creatinine levels were taken. After that, the control group watched a video of people engaged in weight lifting, and the exercise group lifted 6 kg dumbbells (3 kg per arm) for 15 minutes with a 20-second break period after every 2 minutes of performing the exercise or watching the video. After the first session, a 30-minute recuperation period was given before the commencement of the second session (rope jumping). The same procedure was repeated in the second session. Blood pressure, pulse rate, blood glucose, and body temperature were measured immediately after the first session, 15, 30 minutes after the first session, immediately after the second session, 15, and 30 minutes after the second session. Pulmonary indices and urine samples were taken immediately after the first session, 30 minutes after the first session, immediately after the second session, and 30 minutes after the second session.

      Results

      The results showed a significant increase in systolic blood pressure, mean arterial pressure, pulse rate, and body temperature; however, there was no significant difference in diastolic blood pressure, lung function parameters, or blood glucose in the exercise group compared to the control group. In addition, the exercise group showed a significant increase in urine sodium and potassium levels, as well as a significant decrease in urine creatinine level, at the end of the 30-minute recuperation period compared to the control group.

      Conclusion

      The study demonstrated that weightlifting and rope jumping exercise sessions significantly increased blood pressure, pulse rate, and body temperature, but had no significant effect on lung function and blood glucose level. These findings suggest that weightlifting and rope jumping have short-term effects on cardiovascular functions and body temperature, but do not alter lung function or blood glucose level in healthy young males. Significant changes may occur in lung function and blood glucose levels in a long-term study.

    • Expression of PIM1/ASK1 Molecular Pathway Related Genes in Ischemic Cardiomyopathy

      https://doi.org/10.2174/011871529X366280250526131550
      Introduction

      Myocardial ischemia/reperfusion injuries (MI/RI) are responsible for fatal cardiovascular diseases. Myocardial infarction may lead to ischemic cardiomyopathy (ICM). Thereby, illustrating the MI/RI molecular basis could lead to the emergence of novel therapeutic options. pathway is well-known in renal ischemia/ reperfusion. protein can promote autophagy after hypoxia.

      Materials and Methods

      We selected the dataset GSE46224 from the National Center of Biotechnology Information (NCBI) Gene Expression Omnibus (GEO) database for evaluation. This dataset was analyzed using tools such as the Kyoto Encyclopedia of Genes and Genomes, GeneCodis, and BioGRID. Three groups of patients were selected from the dataset. ICM group (n=8), non-failing (NF) group (n=8), and non-ischemic cardiomyopathy (NICM) group (n=8) evaluated for 15 genes expression levels. P-value <0.05 is statistically significant.

      Results

      showed significantly lower gene expression in the ICM group compared to the NF group (-value = 0.012, difference = -6.24). was also significantly down-regulated in the ICM group compared to the NF group (-value =0.0159, difference = -1.478). In contrast, and NF-κB were significantly up-regulated in the ICM group (STAT5B: -value = 0.0238, difference = 2.388; NF-κB: -value = 0.0158, difference = 1.11). The analysis of differences and the volcano plot confirmed these findings, highlighting key dysregulated genes in ICM.

      Conclusion

      In conclusion, ICM patients have altered expression compared to NF individuals. The significant down-regulation of and , along with the up-regulation of and NF-κB, suggests that targeting could be an important strategy to ameliorate ischemia-related cardiomyocyte damage.

    • Reduced Erythrocyte Opsonization by Calreticulin, Lactadherin, Mannose-binding Lectin, and Thrombospondin-1 in MAFLD Patients

      https://doi.org/10.2174/011871529X381576250613041457
      Introduction

      Metabolism dysfunction associated with fatty liver disease During metabolic hepatic inflammation (MAFLD), is characterized by systemic metabolism deregulation leading to increased hepatic erythrophagocytosis and subsequent iron overload and ferroptosis. Studies in animal models have shown that erythrocyte phosphatidylserine exposure drives erythrophagocytosis. However, the mechanism of erythrophagocytosis in human MAFLD has not been fully elucidated yet. Therefore, in this study, we explored the opsonins recognizing phosphatidylserine. In particular, we measured the levels of erythrocyte calreticulin, lactadherin, mannose-binding lectin, and thrombospondin-1.

      Methods

      Twenty-four patients (15 men and 9 women) with MAFLD and 9 healthy controls (4 men and 5 women) were enrolled. Erythrocytes were isolated from EDTA-containing blood through multiple centrifugations and isotonic buffer. Protein levels were measured in erythrocyte lysates (triton X-100 0.1% v/v) or plasma with enzyme-linked immunosorbent assays.

      Results

      Erythrocyte TSP-1 levels were reduced in MAFLD patients. This reduction was not followed by changes in plasma TSP-1 levels or erythrocyte calreticulin, lactadherin, and mannose-binding protein.

      Discussion

      Our results suggest that erythrophagocytosis in human MALFD, unlike animal models, is not mediated by opsonization of exposed phosphatidylserine.

      Conclusion

      Our study underlines the need for disease models that could better reflect the molecular pathogenesis of human MAFLD.

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