ASSESSMENT OF THE RELATIONSHIP BETWEEN SERUM TWEAK LEVELS AND THE DEGREE OF VASCULAR INVOLVEMENT IN PATIENTS WITH STABLE ANGINA PECTORIS
Abstract
Introduction: This study investigates the relationship between serum TWEAK levels and the degree of vascular involvement in patients with stable angina pectoris, offering insights beyond conventional cardiovascular risk factors.
Materials and Methods: This study involved 88 patients (33 women, 55 men) diagnosed with stable angina pectoris. Patients were classified based on angiographic findings. Comprehensive demographic and medical history data were collected, and morning blood samples were analyzed, focusing on TWEAK and IL-6 levels. To assess the severity of coronary artery lesions, a modified version of the Gensini scoring system was employed.
Results: Analyses revealed no significant correlation between TWEAK levels and the severity of coronary artery disease. Although some variations in biochemical markers were observed based on gender and diabetic status, these differences did not exhibit a statistically significant relationship with the degree of vascular involvement.
Conclusion: The findings indicate that serum TWEAK levels do not have a significant association with the severity of vascular involvement in patients with stable angina pectoris. These results highlight the limited efficacy of TWEAK as a sole biomarker in assessing the severity of coronary artery disease, emphasizing the complexity of its role.
References
Gaidai O, Cao Y, Loginov S. Global cardiovascular diseases death rate prediction. Curr Probl Cardiol. 2023;48(5):101622. doi:10.1016/j.cpcardiol.2023.101622
Paripović D, Vukomanovic G, Čivčić M, Peco-Antić A. Predıctors of carotıd ıntıma medıa thıckness ın obese adolescents. Sanamed. 2017;12(1):15-20. doi:10.24125/sanamed.v1i1.174.
Galeone A, Grano M, Brunetti G. Tumor necrosis factor family members and myocardial ischemia-reperfusion injury: state of the art and therapeutic implications. Int J Mol Sci. 2023;24(5):4606. doi:10.3390/ijms24054606.
Nitz K, Herrmann J, Lerman A, Lutgens E. Costimulatory and coinhibitory immune checkpoints in atherosclerosis: therapeutic targets in atherosclerosis? JACC: Basic to Translational Science. Published online 2024. doi:10.1016/j.jacbts.2023.12.007.
Abós B, Pérez-Fernández E, Morel E, Perdiguero P, Tafalla C. Pro-Inflammatory and B Cell Regulating Capacities of TWEAK in Rainbow Trout (Oncorhynchus mykiss). Front Immunol. 2021;12:748836. doi:10.3389/fimmu.2021.748836.
Stephan D, Sbai O, Wen J, Couraud PO, Putterman C, Khrestchatisky M, et al. TWEAK/Fn14 pathway modulates properties of a human microvascular endothelial cell model of blood brain barrier. Journal of Neuroinflammation. 2013;10(1):781. doi:10.1186/1742-2094-10-9.
Hénaut L, Sanz AB, Martin-Sanchez D, Carrasco S, Villa-Bellosta R, Aldamiz-Echevarria G, et al. TWEAK favors phosphate-induced calcification of vascular smooth muscle cells through canonical and non-canonical activation of NFκB. Cell Death Dis. 2016;7(7):e2305. doi:10.1038/cddis.2016.220.
Chen L, Mei W, Song J, Chen K, Ni W, Wang L, et al. CD163 protein inhibits lipopolysaccharide-induced macrophage transformation from M2 to M1 involved in disruption of the TWEAK-Fn14 interaction. Heliyon. 2023;10(1):e23223. doi: 10.1016/j.heliyon.2023.e23223.
Haybar H, Bandar B, Torfi E, Mohebbi A, Saki N. Cytokines and their role in cardiovascular diseases. Cytokine. 2023;169:156261. doi:10.1016/j.cyto.2023.156261.
Landecho MF, Tuero C, Valentí V, Bilbao I, de la Higuera M, Frühbeck G. Relevance of Leptin and Other Adipokines in Obesity-Associated Cardiovascular Risk. Nutrients. 2019;11(11):2664. doi:10.3390/nu11112664.
Hou G, Wang X, Wang A, Yuan L, Zheng Q, Xiao H, et al. The role of secreted proteins in efferocytosis. Front Cell Dev Biol. 2024;11:1332482. doi:10.3389/fcell.2023.1332482.
Urbonaviciene G, Martin-Ventura JL, Lindholt JS, Urbonavicius S, Moreno JA, Egido J, et al. Impact of soluble TWEAK and CD163/TWEAK ratio on long-term cardiovascular mortality in patients with peripheral arterial disease. Atherosclerosis. 2011;219(2):892-9. doi:10.1016/j.atherosclerosis.2011.09.016.
Fernández-Laso V, Sastre C, Valdivielso JM, Fernández E, Martín-Ventura JL, Egido J, et al. Soluble TWEAK levels predict the presence of carotid atherosclerotic plaques in subjects free from clinical cardiovascular diseases. Atherosclerosis. 2015;239(2):358-63. doi:10.1016/j.atherosclerosis.2015.01.040.
Fernández-Laso V, Sastre C, Valdivielso JM, Betriu A, Fernández E, Egido J, et al. Soluble TWEAK and major adverse cardiovascular events in patients with CKD. Clin J Am Soc Nephrol. 2016;11(3):413-22. doi:10.2215/CJN.07900715.
Chorianopoulos E, Jarr K, Steen H, Giannitsis E, Frey N, Katus HA. Soluble TWEAK is markedly upregulated in patients with ST-elevation myocardial infarction and related to an adverse short-term outcome. Atherosclerosis. 2010;211(1):322-6. doi:10.1016/j.atherosclerosis.2010.02.016.
Filusch A, Zelniker T, Baumgärtner C, Eschricht S, Frey N, Katus HA, et al. Soluble TWEAK predicts hemodynamic impairment and functional capacity in patients with pulmonary arterial hypertension. Clin Res Cardiol. 2011;100(10):879-85. doi:10.1007/s00392-011-0318-z.
Blanco-Colio L. TWEAK/Fn14 Axis: A promising target for the treatment of cardiovascular diseases. Front Immunol. 2014;5:3. doi:10.3389/fimmu.2014.00003.
Méndez-Barbero N, Gutiérrez-Muñoz C, Blázquez-Serra R, Martín-Ventura JL, Blanco-Colio LM. Tumor Necrosis Factor-Like Weak Inducer of apoptosis (TWEAK)/Fibroblast Growth Factor-Inducible 14 (Fn14) Axis in cardiovascular diseases: progress and challenges. Cells. 2020;9(2):405. doi:10.3390/cells9020405.
Ratajczak W, Atkinson SD, Kelly C. The TWEAK/Fn14/CD163 axis-implications for metabolic disease. Rev Endocr Metab Disord. 2022;23(3):449-62. doi:10.1007/s11154-021-09688-4.
Xu T, Holzapfel C, Dong X, Bader E, Yu Z, Prehn C, et al. Effects of smoking and smoking cessation on human serum metabolite profile: results from the KORA cohort study. BMC Medicine. 2013;11(1):60. doi:10.1186/1741-7015-11-60.
Copyright (c) 2024 Sanamed
This work is licensed under a Creative Commons Attribution 4.0 International License.
Journal Sanamed is published under an Open Access license. All its content is available free of charge. Users can read, download, copy, distribute, print, search the full text of articles, as well as establish HTML links to them, without having to seek the consent of the author or publisher.
The right to use content without consent does not release the users from the obligation to give the credit to the journal and its content in a manner described under CC BY.