Journals / Archives of Clinical and Experimental Medicine / 2019 / Cilt: 4 - Sayı: 1

Thymosin beta-4 A/T polymorphism and acute coronary syndrome risk

Timozin beta-4 A/T polimorfizmi ve akut koroner sendrom riski

Pages
17–20
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Conclusion: It can be concluded that carrying the Tβ4 A/T (rs75112573) gene polymorphism AT genotype and the A allele may increase risk of ACS.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Aim: Acute coronary syndrome (ACS) describes all the clinical conditions due to myocardial infarction that is caused by decreased blood flow in the coronary artery.
📊
Key Findings & Data:Thymosin beta-4 (Tβ4) plays a significant role in the recovery of damaged tissues and promoting the survival of cardiomyocytes in ACS.
💡
Conclusion & Impact:Conclusion: It can be concluded that carrying the Tβ4 A/T (rs75112573) gene polymorphism AT genotype and the A allele may increase risk of ACS.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Timozin beta-4 (Tβ4) A/T · polimorfizm · akut koroner sendrom

Abstract

Aim: Acute coronary syndrome (ACS) describes all the clinical conditions due to myocardial infarction that is caused by decreased blood flow in the coronary artery. Thymosin beta-4 (Tβ4) plays a significant role in the recovery of damaged tissues and promoting the survival of cardiomyocytes in ACS. In this study, it was aimed to determine the Tβ4 A/T (rs75112573) variation in ACS and its effects on the disease. Methods: This was a prospective case-control study. Forty-eight patients with ACS and 45 healthy controls were recruited for this study. Genetic analysis was performed using polymerase chain reaction/restriction fragment length polymorphism (PCR/RFLP).Results: The AT genotype (p<0.001, X2:12.40, OR:5.42, 95% CI:2.02-14.53) and the A allele (p<0.001, X2:17.22, OR:6.66, 95% CI:2.61-16.98) frequency was found significantly higher in the patient group, while in the control group the TT genotype was statistically higher (p<0.001, X2:17.22, OR:2.13, 95% CI:1.44-3.16). LDL-cholesterol levels in the patient group (p<0.001, 95% CI:30.12-55.90), and HDL-cholesterol levels in the control group (p<0.001, 95% CI:5.30-15.34) were significantly higher. In the patient group, total cholesterol and HDL-cholesterol levels were found significantly higher in AT genotype carriers compared to the AA genotype carriers (p=0.036, 95% CI:0.59-17.25), while VLDL-cholesterol levels were higher in the AA genotype carriers compared to the AT (p=0.011, 95% CI:6.73-49.86), and TT (p=0.018, 95% CI:4.95-49.49) genotype carriers. Conclusion: It can be concluded that carrying the Tβ4 A/T (rs75112573) gene polymorphism AT genotype and the A allele may increase risk of ACS.

Özet

Amaç: Akut koroner sendrom (ACS), koroner arter kan akımının azalması sonucu miyokard iskemisinin neden olduğu klinik tabloların tamamını ifade eder. Thymosin beta-4 geni (Tβ4) hasarlı dokuların iyileşmesinde ve ACS’de kardiyomiyositlerin canlı kalmasında önemli rol oynamaktadır. Bu çalışmada ACS’li hastaların Tβ4 genindeki A/T (rs75112573) varyasyonunun tespit edilmesi ve akut koroner hastalığına olan etkilerinin belirlenmesi amaçlanmıştır. Yöntemler: Bu prospektif bir vaka kontrol çalışmasıdır. Çalışmaya ACS'li 48 hasta ve 45 sağlıklı kontrol birey dahil edildi. Genetik analiz, polimeraz zincir reaksiyonu/restriksiyon parça uzunluk polimorfizmi (PCR / RFLP) yöntemleri kullanılarak yapıldı.Bulgular: Kontrol grubu ile karşılaştırıldığında hasta grubunda AT genotipi (p<0.001, X2:12.40, OR:5.42, %95 CI:2.02-14.53) ve A alleli (p<0.001, X2:17.22, OR:6.66, %95 CI:2.61-16.98) taşıma sıklığı anlamlı olarak yükselmiştir. Kontrol grubunda ise TT genotip sıklığının hasta grubuna göre istatistiksel olarak yüksek olduğu gözlemlenmiştir (p<0.001, X2:17.22, OR:2.13, %95 CI:1.44-3.16). Hasta grubumuzun LDL-kolesterol seviyesi (p<0.001, %95 CI:30.12-55.90), kontrol grubumuzun ise HDL-kolesterol seviyesi yüksek bulunmuştur (p<0.001, %95 CI:5.30-15.34). Hasta grubunda AT genotipi taşıyanlarda AA genotipi taşıyanlara göre kolesterol ve HDL-kolestrol düzeyleri anlamlı derecede yüksek olarak bulunmuştur (p=0.036, %95 CI:0.59-17.25). VLDL-kolestreol düzeyleri ise hasta grubunda AA genotipi taşıyanlarda, AT (p=0.011, %95 CI:6.73-49.86) ve TT (p=0.018, %95 CI:4.95-49.49) genotipi taşıyanlara göre anlamlı şekilde yükselmiştir. Sonuç: Tβ4 A/T (rs75112573) gene polymorphism için AT genotipi ve A alleli taşımanın ACS riskini artırabileceği sonucuna ulaşılabilir.

🔖

Cite This Article

GEZEN, M., YILMAZ, Ü., FAZLIOĞULLARI, O., YİLMAZ, N., HOROZOĞLU, C., ERGEN, A., ZEYBEK, Ş. Ü. (2019). Thymosin beta-4 A/T polymorphism and acute coronary syndrome risk. Archives of Clinical and Experimental Medicine, Cilt: 4 - Sayı: 1, 17–20. https://ajindex.com/articles/142491

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (14)

  1. Moodie DS. The Global Burden of Cardiovascular Disease. Congenit Heart Dis. 2016
  2. American College of Cardiology/American Heart Association Task Force on Practice G. ACC/AHA guidelines for the management of patients with unstable angina and non-ST segment elevation myocardial infarction: executive summary and recommendations. Catheter Cardiovasc Interv. 2000
  3. Coskun A, Eren SH, Korkmaz I, Guven FMK. The epidemiological and prognostic importance of the aVR lead among patients with and without ST segment elevation. Turk Gogus Kalp Damar Cerrahisi Dergisi-Turkish J Thorac Cardiovasc Surg. 2011
  4. Van de Werf F, Ardissino D, Betriu A, Cokkinos DV, Falk E, Fox KA, et al. Management of acute myocardial infarction in patients presenting with ST-segment elevation. The Task Force on the Management of Acute Myocardial Infarction of the European Society of Cardiology. Eur Heart J. 2003
  5. Kumar A, Cannon CP. Acute coronary syndromes: diagnosis and management, part I. Mayo Clin Proc. 2009
  6. Smith JN, Negrelli JM, Manek MB, Hawes EM, Viera AJ. Diagnosis and management of acute coronary syndrome: an evidence-based update. J Am Board Fam Med. 2015
  7. Shrivastava S, Srivastava D, Olson EN, DiMaio JM, Bock-Marquette I. Thymosin beta4 and cardiac repair. Ann N Y Acad Sci. 2010
  8. Goldstein AL, Hannappel E, Kleinman HK. Thymosin beta4: actin-sequestering protein moonlights to repair injured tissues. Trends Mol Med. 2005
  9. Yesilay AB, Karakurt O, Akdemir R, Erden G, Kilic H, Acikel S, et al. Thymosin beta4 levels after successful primary percutaneous coronary intervention for acute myocardial infarction. Turk Kardiyol Dern Ars. 2011
  10. Sosne G, Qiu P, Kurpakus-Wheater M. Thymosin beta 4: A novel corneal wound healing and anti-inflammatory agent. Clin Ophthalmol. 2007
  11. Bock-Marquette I, Saxena A, White MD, Dimaio JM, Srivastava D. Thymosin beta4 activates integrin-linked kinase and promotes cardiac cell migration, survival and cardiac repair. Nature. 2004
  12. Crockford D. Development of thymosin beta4 for treatment of patients with ischemic heart disease. Ann N Y Acad Sci. 2007
  13. Miller SA, Dykes DD, Polesky HF. A simple salting out procedure for extracting DNA from human nucleated cells. Nucleic Acids Res. 1988
  14. Kilic S, Simsek E, Soner Kemal H, Yuce EI, Turkoglu C, Kayikcioglu M. The role of specialized prevention clinics for the shor