Research Article
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Exploration of the Relationship Between Routine Biochemistry Parameters, Scavenger Receptors, and Apoptotic Proteins During the Treatment Process of Acute Myocardial Infarction

Year 2024, Volume: 13 Issue: 1, 370 - 381, 27.03.2024
https://doi.org/10.37989/gumussagbil.1321191

Abstract

In this study, we aimed to investigate how the stent treatment process affects scavenger receptors and apoptotic protein levels in patients with myocardial infarction clinical picture. In this context, patients without coronary occlusive lesion on coronary angiography were included in the control group, and patients coronary occlusive lesion on coronary angiography were included in the infarction group. Routine biochemistry and cardiac markers from serum samples were measured with a biochemistry autoanalyzer. Blood samples were collected from the control group and patients with myocardial infarction (day 0, day 3 and day 30) and PBMCs were isolated with ficoll solution. LOX-1, CD36, CD68 and CXCL16 gene expressions in PBMCs were determined via qPCR. In addition, BAX, BCL-2 and Caspase-3 protein levels in serum samples were measured by ELISA method. When the results were evaluated, no significant difference was found between the groups in the routine biochemistry values for triglyceride, cholesterol and LDL. HDL levels were lower in the MI group. Conversely, glucose levels were higher in the MI group. Besides, cardiac markers, including troponin, CK-MB and creatine kinase, showed a significant increase in the MI group. However, there was no significant change in the gene expressions of LOX-1, CD36, CD68, and CXCL16 in PBMCs both between the control group and the MI group and between time-dependent MI groups (day 0, day 3 and day 30). Similarly, no significant changes were observed in the protein expressions of BAX, BCL-2 and Caspase-3. The non-significant difference in the expressions of scavenger receptors may possibly be due to the similarity of the lipid profile observed between the groups.

References

  • 1. Thygesen, K, Alpert, J.S. and White, H.D. (2007). “Universal Definition of Myocardial Infarction’’. Circulation, 116 (22), 2634-2653.
  • 2. Anderson, J.L. and Morrow, D.A. (2017). “Acute Myocardial Infarction’’. The New England Journal of Medicine, 376 (21), 2053–2064.
  • 3. Mozaffarian, D, Benjamin, E.J, Go, A.S, Arnett, D.K, Blaha, M.J, Cushman, M. and American Heart Association Statistics Committee and Stroke Statistics Subcommittee. (2015). “Heart disease and stroke statistics--2015 update: a Report from the American Heart Association’’. Circulation, 131 (4), 29–322.
  • 4. WHO. Erişim adresi: https://www.who.int/news-room/fact-sheets/detail/cardiovascular-diseases-(cvds) (Erişim tarihi: 24.05.2022).
  • 5. Bostan, M.M, Stătescu, C, Anghel, L, Șerban, I.L, Cojocaru, E. and Sascău, R. (2020). “Post-Myocardial Infarction Ventricular Remodeling Biomarkers-The Key Link between Pathophysiology and Clinic’’. Biomolecules, 10 (11), 1-22.
  • 6. Kon, V, Yang, H. and Fazio, S. (2015). “Residual cardiovascular risk in chronic kidney disease: role of high-density lipoprotein”. Archives of Medical Research, 46 (5), 379-391.
  • 7. Stapleton, P.A, Goodwill, A.G, James, M.E, Brock, R.W. and Frisbee, J.C. (2010). “Hypercholesterolemia and microvascular dysfunction: interventional strategies”. Journal of Inflammation, 7, 1-10.
  • 8. Zani, I.A, Stephen, S.L, Mughal, N.A, Russell, D, Homer-Vanniasinkam, S, and Wheatcroft, S.B. (2015). “Scavenger Receptor Structure and Function in Health and Disease’’. Cells, 4 (2), 178–201.
  • 9. Kennedy, D.J, Chen, Y, Huang, W, Viterna, J, Liu, J. and Westfall, K. (2013). “CD36 and Na/K-ATPase-α1 form a Proinflammatory Signaling Loop in Kidney’’. Hypertension, 61 (1), 216-224.
  • 10. Eom, M, Hudkins, K.L. and Alpers, C. E. (2015). “Foam Cells and the Pathogenesis of Kidney Disease’’. Current Opinion in Nephrology and Hypertension, 24 (3), 245-251.
  • 11. Meier, S.M, Wultsch, A, Hollaus, M, Ammann, M, Pemberger, E. and Liebscher, F. (2015). “Effect of chronic kidney disease on macrophage cholesterol efflux’’. Life Sciences, 136, 1-6.
  • 12. Gupta, S, Kass, G.E, Szegezdi, E. and Joseph, B. (2009). “The Mitochondrial Death Pathway: A Promising Therapeutic Target in Diseases’’. Journal of Cellular and Molecular Medicine, 13 (6), 1004-1033.
  • 13. Brunelle, J.K. and Letai, A. (2009). “Control of Mitochondrial Apoptosis by the Bcl-2 Family’’. Journal of Cell Science, 122 (4), 437-441.
  • 14. Hochman, A, Sternin, H, Gorodin, S, Korsmeyer, S, Ziv, I. and Melamed, E. (1998). “Enhanced Oxidative Stress and Altered Antioxidants in Brains of Bcl-2-deficient Mice’’. Journal of Neurochemistry, 71 (2), 741-748.
  • 15. Kubli, D.A, Quinsay, M.N, Huang, C, Lee, Y. and Gustafsson, A.B. (2008). “Bnip3 functions as a mitochondrial sensor of oxidative stress during myocardial ischemia and reperfusion’’. The American Journal of Physiology-Heart and Circulatory Physiology, 295 (5), 2025-2031.
  • 16. Favaloro, B, Allocati, N, Graziano, V, Di Ilio, C. and De Laurenzi, V. (2012). “Role of Apoptosis in Disease’’. Aging (Albany NY), 4 (5), 330-349.
  • 17. Kültürsay, H. ve Kayıkçıoğlu, M. (2002). “Apoptozis ve Kardiyovasküler Hastalıklar’’. Anadolu Kardiyoloji Dergisi, 4, 323-329.
  • 18. Van de Werf, F, Bax, J, Betriu, A, Blomstrom-Lundqvist, C, Crea, F. and Falk, V. (2008). “Management of Acute Myocardial Infarction in Patients Presenting with Persistent ST-segment Elevation: The Task Force on the Management of ST-Segment Elevation Acute Myocardial Infarction of the European Society of Cardiology’’. European Heart Journal, 29 (23), 2909–2945.
  • 19. Gollapudi, R.R, Teirstein, P.S, Stevenson, D.D. and Simon, R.A. (2004). “Aspirin Sensitivity: Implications for Patients with Coronary Artery Disease’’. Journal of the American Medical Association, 292 (24), 3017–3023.
  • 20. Madhavan, M.V, Redfors, B, Ali, Z.A, Prasad, M, Shahim, B. and Smits, P.C. (2020). “Long-Term Outcomes After Revascularization for Stable Ischemic Heart Disease: An Individual Patient-Level Pooled Analysis of 19 Randomized Coronary Stent Trials. Circulation’’. Cardiovascular Interventions, 13 (4), 1-8.
  • 21. Aydin, S, Ugur, K, Aydin, S, Sahin, İ. and Yardim, M. (2019). “Biomarkers in acute myocardial infarction: current perspectives.” Vascular Health and Risk Management, 15, 1-10.
  • 22. Mehta, J.L, Sanada, N, Hu, C.P, Chen, J, Dandapat, A. and Sugawara, F. (2007). “Deletion of LOX-1 Reduces Atherogenesis in LDLR Knockout Mice Fed High Cholesterol Diet’’. Circulation Research, 100 (11), 1634-1642.
  • 23. Guo, X, Xiang, Y, Yang, H, Yu, L, Peng, X. and Guo, R. (2017). “Association of the LOX-1 rs1050283 Polymorphism with Risk for Atherosclerotic Cerebral Infarction and its Effect on sLOX-1 and LOX-1 Expression in a Chinese Population’’. Journal of Atherosclerosis and Thrombosis, 24 (6), 572–582.
  • 24. Lu, J, Wang, X, Wang, W, Muniyappa, H, Hu, C. and Mitra, S. (2012). “LOX-1 Abrogation Reduces Cardiac Hypertrophy and Collagen Accumulation Following Chronic Ischemia in the Mouse’’. Gene Therapy, 19 (5), 522–531.
  • 25. Wang, J. and Li, Y. (2019). “CD36 Tango in Cancer: Signaling Pathways and Functions’’. Theranostics, 9 (17), 4893–4908.
  • 26. Yazgan, B, Sozen, E, Karademir, B, Ustunsoy, S, Ince, U. and Zarkovic, N. (2018). “CD36 Expression in Peripheral Blood Mononuclear Cells Reflects the onset of Atherosclerosis’’. BioFactors (Oxford, England), 44 (6), 588–596.
  • 27. Ackers, I, Szymanski, C, Duckett, K.J, Consitt, L.A, Silver, M.J. and Malgor, R. (2018). “Blocking Wnt5a Signaling Decreases CD36 Expression and foam Cell Formation in Atherosclerosis’’. Cardiovascular Pathology: The Official Journal of the Society for Cardiovascular Pathology, 34, 1–8.
  • 28. Song, L, Lee, C. and Schindler, C. (2011). “Deletion of the Murine Scavenger Receptor CD68’’. Journal of Lipid Research, 52 (8), 1542–1550.
  • 29. Zeibig, S, Li, Z, Wagner, S, Holthoff, H.P, Ungerer, M. and Bültmann, A. (2011). “Effect of the oxLDL Binding Protein Fc-CD68 on Plaque Extension and Vulnerability in Atherosclerosis’’. Circulation Research, 108 (6), 695–703.
  • 30. Gursel, M, Gursel, I, Mostowski, H.S. and Klinman, D.M. (2006). “CXCL16 Influences the Nature and Specificity of CpG-induced Immune Activation. Journal of Immunology (Baltimore, Md: 1950), 177 (3), 1575–1580.
  • 31. Sheikine, Y. and Sirsjö, A. (2008). “CXCL16/SR-PSOX--a Friend or a Foe in Atherosclerosis’’. Atherosclerosis, 197 (2), 487–495.
  • 32. Liu, X. (2021). “Changes and Significance of Serum CXCL-16, GDF-15, PLA-2 Levels in Patients with Cerebral Infarction’’. American Journal of Translational Research, 13 (5), 5617–5622.
  • 33. Cheng, Y.C, Chang, M, Tsai, C.C, Chen, T.S, Fan, C.C. and Lin, C. (2013). “Garlic Oil Attenuates the Cardiac Apoptosis in Hamster-fed with Hypercholesterol Diet’’. Food Chemistry, 136 (3-4), 1296–1302.
  • 34. Osipov R.M, Bianchi, C, Feng, J, Clements, R.T, Liu, Y. and Robich, M.P. (2009). “Effect of Hypercholesterolemia on Myocardial Necrosis and Apoptosis in the Setting of Ischemia-Reperfusion’’. Circulation, 120 (11), 22-30.
  • 35. Zheng, X, Zhong, T, Ma, Y, Wan, X, Qin, A. and Yao, B. (2020). “Bnip3 Mediates Doxorubicin-induced Cardiomyocyte Pyroptosis Via Caspase-3/GSDME’’. Life Sciences, 242, 1-9.
  • 36. Yazgan, B, Ustunsoy, S, Karademir, B. and Kartal Ozer, N. (2014). “CD36 as a biomarker of atherosclerosis.” Free Radical Biology and Medicine, 75, 10.
  • 37. Zhang, J, Ding, W, Liu, J, Wan, J. and Wang, M. (2023). “Scavenger Receptors in Myocardial Infarction and Ischemia/Reperfusion Injury: The Potential for Disease Evaluation and Therapy.” Journal of the American Heart Association, 12 (2), 1-16.
  • 38. Sozen, E, Yazgan, B, Sahin, A, Ince, U. and Kartal Ozer, N. (2018). “High cholesterol diet-induced changes in oxysterol and scavenger receptor levels in heart tissue.” Oxidative Medicine and Cellular Longevity, 2018, 1-13.

Akut Miyokard İnfarktüsü Tedavi Sürecinde Rutin Biyokimya Parametreleri, Çöpçü Reseptörler ve Apoptotik Proteinler Arasındaki İlişkinin İncelenmesi

Year 2024, Volume: 13 Issue: 1, 370 - 381, 27.03.2024
https://doi.org/10.37989/gumussagbil.1321191

Abstract

Bu çalışmada miyokard infarktüsü klinik tablosuna sahip hastalarda stent tedavi sürecinin çöpçü reseptörler ve apoptotik protein düzeylerine nasıl etki gösterdiğinin incelenmesi amaçlanmıştır. Bu amaçla koroner anjiyografide koroner tıkayıcı lezyonu olmayanlar kontrol grubuna ve koroner anjiyografide belirgin koroner tıkayıcı lezyonu ile birlikte miyokard infarktüsü klinik tablosu bulunan hastalar infarktüs grubuna alınmıştır. Serum örneklerinden rutin biyokimya ve kardiyak belirteçler biyokimya otoanalizörü ile ölçülmüştür. Kontrol grubu ve Miyokard infarktüsü geçiren hastalardan (0. gün, 3. gün ve 30. gün) kan örnekleri alınmış ve PBMC’ler ficoll solüsyonuyla izole edilmiştir. PBMC’lerde LOX-1, CD36, CD68 ve CXCL16 gen ekspresyonları qPCR yöntemi ile belirlenmiştir. Ayrıca serum örneklerindeki BAX, BCL-2 ve Kaspaz-3 protein seviyeleri ELISA yöntemi ile ölçülmüştür. Sonuçlar değerlendirildiğinde rutin biyokimya değerlerinden trigliserid, kolesterol ve LDL kolesterol değerlerinde gruplar arasında anlamlı bir fark bulunamamıştır. HDL kolesterol Mİ gruplarında daha düşük bulunmuştur. Glukoz ise Mİ grubunda daha yüksek bulunmuştur. Mİ grubunda kardiyak belirteçler olan troponin, CK-MB ve kreatin kinaz değerleri anlamlı bir artış göstermiştir. Ancak hem kontrol grubu ile Mİ grubu arasında hem de Mİ grubunda zamana bağlı (0. gün, 3. gün ve 30. gün) PBMC’lerin LOX-1, CD36, CD68 ve CXCL16 gen ekspresyonlarında anlamlı bir değişim bulunamamıştır. Benzer olarak serum BAX, BCL-2 ve Kaspaz-3 protein ekspresyonlarında da önemli bir değişiklik gözlenmemiştir. Çöpçü reseptör ekspresyonlarında anlamlı bir artışın olmaması muhtemelen gruplar arasındaki benzer lipid profilinin gözlenmesinden kaynaklanabilir.

References

  • 1. Thygesen, K, Alpert, J.S. and White, H.D. (2007). “Universal Definition of Myocardial Infarction’’. Circulation, 116 (22), 2634-2653.
  • 2. Anderson, J.L. and Morrow, D.A. (2017). “Acute Myocardial Infarction’’. The New England Journal of Medicine, 376 (21), 2053–2064.
  • 3. Mozaffarian, D, Benjamin, E.J, Go, A.S, Arnett, D.K, Blaha, M.J, Cushman, M. and American Heart Association Statistics Committee and Stroke Statistics Subcommittee. (2015). “Heart disease and stroke statistics--2015 update: a Report from the American Heart Association’’. Circulation, 131 (4), 29–322.
  • 4. WHO. Erişim adresi: https://www.who.int/news-room/fact-sheets/detail/cardiovascular-diseases-(cvds) (Erişim tarihi: 24.05.2022).
  • 5. Bostan, M.M, Stătescu, C, Anghel, L, Șerban, I.L, Cojocaru, E. and Sascău, R. (2020). “Post-Myocardial Infarction Ventricular Remodeling Biomarkers-The Key Link between Pathophysiology and Clinic’’. Biomolecules, 10 (11), 1-22.
  • 6. Kon, V, Yang, H. and Fazio, S. (2015). “Residual cardiovascular risk in chronic kidney disease: role of high-density lipoprotein”. Archives of Medical Research, 46 (5), 379-391.
  • 7. Stapleton, P.A, Goodwill, A.G, James, M.E, Brock, R.W. and Frisbee, J.C. (2010). “Hypercholesterolemia and microvascular dysfunction: interventional strategies”. Journal of Inflammation, 7, 1-10.
  • 8. Zani, I.A, Stephen, S.L, Mughal, N.A, Russell, D, Homer-Vanniasinkam, S, and Wheatcroft, S.B. (2015). “Scavenger Receptor Structure and Function in Health and Disease’’. Cells, 4 (2), 178–201.
  • 9. Kennedy, D.J, Chen, Y, Huang, W, Viterna, J, Liu, J. and Westfall, K. (2013). “CD36 and Na/K-ATPase-α1 form a Proinflammatory Signaling Loop in Kidney’’. Hypertension, 61 (1), 216-224.
  • 10. Eom, M, Hudkins, K.L. and Alpers, C. E. (2015). “Foam Cells and the Pathogenesis of Kidney Disease’’. Current Opinion in Nephrology and Hypertension, 24 (3), 245-251.
  • 11. Meier, S.M, Wultsch, A, Hollaus, M, Ammann, M, Pemberger, E. and Liebscher, F. (2015). “Effect of chronic kidney disease on macrophage cholesterol efflux’’. Life Sciences, 136, 1-6.
  • 12. Gupta, S, Kass, G.E, Szegezdi, E. and Joseph, B. (2009). “The Mitochondrial Death Pathway: A Promising Therapeutic Target in Diseases’’. Journal of Cellular and Molecular Medicine, 13 (6), 1004-1033.
  • 13. Brunelle, J.K. and Letai, A. (2009). “Control of Mitochondrial Apoptosis by the Bcl-2 Family’’. Journal of Cell Science, 122 (4), 437-441.
  • 14. Hochman, A, Sternin, H, Gorodin, S, Korsmeyer, S, Ziv, I. and Melamed, E. (1998). “Enhanced Oxidative Stress and Altered Antioxidants in Brains of Bcl-2-deficient Mice’’. Journal of Neurochemistry, 71 (2), 741-748.
  • 15. Kubli, D.A, Quinsay, M.N, Huang, C, Lee, Y. and Gustafsson, A.B. (2008). “Bnip3 functions as a mitochondrial sensor of oxidative stress during myocardial ischemia and reperfusion’’. The American Journal of Physiology-Heart and Circulatory Physiology, 295 (5), 2025-2031.
  • 16. Favaloro, B, Allocati, N, Graziano, V, Di Ilio, C. and De Laurenzi, V. (2012). “Role of Apoptosis in Disease’’. Aging (Albany NY), 4 (5), 330-349.
  • 17. Kültürsay, H. ve Kayıkçıoğlu, M. (2002). “Apoptozis ve Kardiyovasküler Hastalıklar’’. Anadolu Kardiyoloji Dergisi, 4, 323-329.
  • 18. Van de Werf, F, Bax, J, Betriu, A, Blomstrom-Lundqvist, C, Crea, F. and Falk, V. (2008). “Management of Acute Myocardial Infarction in Patients Presenting with Persistent ST-segment Elevation: The Task Force on the Management of ST-Segment Elevation Acute Myocardial Infarction of the European Society of Cardiology’’. European Heart Journal, 29 (23), 2909–2945.
  • 19. Gollapudi, R.R, Teirstein, P.S, Stevenson, D.D. and Simon, R.A. (2004). “Aspirin Sensitivity: Implications for Patients with Coronary Artery Disease’’. Journal of the American Medical Association, 292 (24), 3017–3023.
  • 20. Madhavan, M.V, Redfors, B, Ali, Z.A, Prasad, M, Shahim, B. and Smits, P.C. (2020). “Long-Term Outcomes After Revascularization for Stable Ischemic Heart Disease: An Individual Patient-Level Pooled Analysis of 19 Randomized Coronary Stent Trials. Circulation’’. Cardiovascular Interventions, 13 (4), 1-8.
  • 21. Aydin, S, Ugur, K, Aydin, S, Sahin, İ. and Yardim, M. (2019). “Biomarkers in acute myocardial infarction: current perspectives.” Vascular Health and Risk Management, 15, 1-10.
  • 22. Mehta, J.L, Sanada, N, Hu, C.P, Chen, J, Dandapat, A. and Sugawara, F. (2007). “Deletion of LOX-1 Reduces Atherogenesis in LDLR Knockout Mice Fed High Cholesterol Diet’’. Circulation Research, 100 (11), 1634-1642.
  • 23. Guo, X, Xiang, Y, Yang, H, Yu, L, Peng, X. and Guo, R. (2017). “Association of the LOX-1 rs1050283 Polymorphism with Risk for Atherosclerotic Cerebral Infarction and its Effect on sLOX-1 and LOX-1 Expression in a Chinese Population’’. Journal of Atherosclerosis and Thrombosis, 24 (6), 572–582.
  • 24. Lu, J, Wang, X, Wang, W, Muniyappa, H, Hu, C. and Mitra, S. (2012). “LOX-1 Abrogation Reduces Cardiac Hypertrophy and Collagen Accumulation Following Chronic Ischemia in the Mouse’’. Gene Therapy, 19 (5), 522–531.
  • 25. Wang, J. and Li, Y. (2019). “CD36 Tango in Cancer: Signaling Pathways and Functions’’. Theranostics, 9 (17), 4893–4908.
  • 26. Yazgan, B, Sozen, E, Karademir, B, Ustunsoy, S, Ince, U. and Zarkovic, N. (2018). “CD36 Expression in Peripheral Blood Mononuclear Cells Reflects the onset of Atherosclerosis’’. BioFactors (Oxford, England), 44 (6), 588–596.
  • 27. Ackers, I, Szymanski, C, Duckett, K.J, Consitt, L.A, Silver, M.J. and Malgor, R. (2018). “Blocking Wnt5a Signaling Decreases CD36 Expression and foam Cell Formation in Atherosclerosis’’. Cardiovascular Pathology: The Official Journal of the Society for Cardiovascular Pathology, 34, 1–8.
  • 28. Song, L, Lee, C. and Schindler, C. (2011). “Deletion of the Murine Scavenger Receptor CD68’’. Journal of Lipid Research, 52 (8), 1542–1550.
  • 29. Zeibig, S, Li, Z, Wagner, S, Holthoff, H.P, Ungerer, M. and Bültmann, A. (2011). “Effect of the oxLDL Binding Protein Fc-CD68 on Plaque Extension and Vulnerability in Atherosclerosis’’. Circulation Research, 108 (6), 695–703.
  • 30. Gursel, M, Gursel, I, Mostowski, H.S. and Klinman, D.M. (2006). “CXCL16 Influences the Nature and Specificity of CpG-induced Immune Activation. Journal of Immunology (Baltimore, Md: 1950), 177 (3), 1575–1580.
  • 31. Sheikine, Y. and Sirsjö, A. (2008). “CXCL16/SR-PSOX--a Friend or a Foe in Atherosclerosis’’. Atherosclerosis, 197 (2), 487–495.
  • 32. Liu, X. (2021). “Changes and Significance of Serum CXCL-16, GDF-15, PLA-2 Levels in Patients with Cerebral Infarction’’. American Journal of Translational Research, 13 (5), 5617–5622.
  • 33. Cheng, Y.C, Chang, M, Tsai, C.C, Chen, T.S, Fan, C.C. and Lin, C. (2013). “Garlic Oil Attenuates the Cardiac Apoptosis in Hamster-fed with Hypercholesterol Diet’’. Food Chemistry, 136 (3-4), 1296–1302.
  • 34. Osipov R.M, Bianchi, C, Feng, J, Clements, R.T, Liu, Y. and Robich, M.P. (2009). “Effect of Hypercholesterolemia on Myocardial Necrosis and Apoptosis in the Setting of Ischemia-Reperfusion’’. Circulation, 120 (11), 22-30.
  • 35. Zheng, X, Zhong, T, Ma, Y, Wan, X, Qin, A. and Yao, B. (2020). “Bnip3 Mediates Doxorubicin-induced Cardiomyocyte Pyroptosis Via Caspase-3/GSDME’’. Life Sciences, 242, 1-9.
  • 36. Yazgan, B, Ustunsoy, S, Karademir, B. and Kartal Ozer, N. (2014). “CD36 as a biomarker of atherosclerosis.” Free Radical Biology and Medicine, 75, 10.
  • 37. Zhang, J, Ding, W, Liu, J, Wan, J. and Wang, M. (2023). “Scavenger Receptors in Myocardial Infarction and Ischemia/Reperfusion Injury: The Potential for Disease Evaluation and Therapy.” Journal of the American Heart Association, 12 (2), 1-16.
  • 38. Sozen, E, Yazgan, B, Sahin, A, Ince, U. and Kartal Ozer, N. (2018). “High cholesterol diet-induced changes in oxysterol and scavenger receptor levels in heart tissue.” Oxidative Medicine and Cellular Longevity, 2018, 1-13.
There are 38 citations in total.

Details

Primary Language Turkish
Subjects Receptors and Membrane Biology, Medical Biochemistry - Proteins, Peptides and Proteomics
Journal Section Original Article
Authors

Sema Tahtalıoğlu 0000-0001-5289-3224

Abdulkadir Çakmak 0000-0001-7427-3368

Gökhan Keskin 0000-0002-1695-5624

Burak Yazgan 0000-0003-0717-7768

Publication Date March 27, 2024
Published in Issue Year 2024 Volume: 13 Issue: 1

Cite

APA Tahtalıoğlu, S., Çakmak, A., Keskin, G., Yazgan, B. (2024). Akut Miyokard İnfarktüsü Tedavi Sürecinde Rutin Biyokimya Parametreleri, Çöpçü Reseptörler ve Apoptotik Proteinler Arasındaki İlişkinin İncelenmesi. Gümüşhane Üniversitesi Sağlık Bilimleri Dergisi, 13(1), 370-381. https://doi.org/10.37989/gumussagbil.1321191
AMA Tahtalıoğlu S, Çakmak A, Keskin G, Yazgan B. Akut Miyokard İnfarktüsü Tedavi Sürecinde Rutin Biyokimya Parametreleri, Çöpçü Reseptörler ve Apoptotik Proteinler Arasındaki İlişkinin İncelenmesi. Gümüşhane Üniversitesi Sağlık Bilimleri Dergisi. March 2024;13(1):370-381. doi:10.37989/gumussagbil.1321191
Chicago Tahtalıoğlu, Sema, Abdulkadir Çakmak, Gökhan Keskin, and Burak Yazgan. “Akut Miyokard İnfarktüsü Tedavi Sürecinde Rutin Biyokimya Parametreleri, Çöpçü Reseptörler Ve Apoptotik Proteinler Arasındaki İlişkinin İncelenmesi”. Gümüşhane Üniversitesi Sağlık Bilimleri Dergisi 13, no. 1 (March 2024): 370-81. https://doi.org/10.37989/gumussagbil.1321191.
EndNote Tahtalıoğlu S, Çakmak A, Keskin G, Yazgan B (March 1, 2024) Akut Miyokard İnfarktüsü Tedavi Sürecinde Rutin Biyokimya Parametreleri, Çöpçü Reseptörler ve Apoptotik Proteinler Arasındaki İlişkinin İncelenmesi. Gümüşhane Üniversitesi Sağlık Bilimleri Dergisi 13 1 370–381.
IEEE S. Tahtalıoğlu, A. Çakmak, G. Keskin, and B. Yazgan, “Akut Miyokard İnfarktüsü Tedavi Sürecinde Rutin Biyokimya Parametreleri, Çöpçü Reseptörler ve Apoptotik Proteinler Arasındaki İlişkinin İncelenmesi”, Gümüşhane Üniversitesi Sağlık Bilimleri Dergisi, vol. 13, no. 1, pp. 370–381, 2024, doi: 10.37989/gumussagbil.1321191.
ISNAD Tahtalıoğlu, Sema et al. “Akut Miyokard İnfarktüsü Tedavi Sürecinde Rutin Biyokimya Parametreleri, Çöpçü Reseptörler Ve Apoptotik Proteinler Arasındaki İlişkinin İncelenmesi”. Gümüşhane Üniversitesi Sağlık Bilimleri Dergisi 13/1 (March 2024), 370-381. https://doi.org/10.37989/gumussagbil.1321191.
JAMA Tahtalıoğlu S, Çakmak A, Keskin G, Yazgan B. Akut Miyokard İnfarktüsü Tedavi Sürecinde Rutin Biyokimya Parametreleri, Çöpçü Reseptörler ve Apoptotik Proteinler Arasındaki İlişkinin İncelenmesi. Gümüşhane Üniversitesi Sağlık Bilimleri Dergisi. 2024;13:370–381.
MLA Tahtalıoğlu, Sema et al. “Akut Miyokard İnfarktüsü Tedavi Sürecinde Rutin Biyokimya Parametreleri, Çöpçü Reseptörler Ve Apoptotik Proteinler Arasındaki İlişkinin İncelenmesi”. Gümüşhane Üniversitesi Sağlık Bilimleri Dergisi, vol. 13, no. 1, 2024, pp. 370-81, doi:10.37989/gumussagbil.1321191.
Vancouver Tahtalıoğlu S, Çakmak A, Keskin G, Yazgan B. Akut Miyokard İnfarktüsü Tedavi Sürecinde Rutin Biyokimya Parametreleri, Çöpçü Reseptörler ve Apoptotik Proteinler Arasındaki İlişkinin İncelenmesi. Gümüşhane Üniversitesi Sağlık Bilimleri Dergisi. 2024;13(1):370-81.