Ateroskleroz patofizyolojisinde Kruppel Benzeri Faktör 14’ün rolü

Ulaş Değirmenci; Metin Yıldırım; Serap Yalın

doi:10.26559/mersinsbd.675368

Review

Ateroskleroz patofizyolojisinde Kruppel Benzeri Faktör 14’ün rolü

Year 2020, Volume: 13 Issue: 2, 241 - 248, 26.08.2020

Ulaş Değirmenci Metin Yıldırım Serap Yalın

https://doi.org/10.26559/mersinsbd.675368

Abstract

Kardiyovasküler hastalıklar (KVH) dünya genelinde ölümlerin üçte birinden sorumludur. Bu hastalıklarda görülen ortak patolojik durum aterosklerozdur. Ateroskleroz, erken safhalarında endotelyal hücre aktivasyonu/disfonksiyonunun görülmesi sebebiyle inflamatuar bir hastalık olarak nitelendirilmektedir. Ateroskleroz patolojisinin kötü kolesterol olarak bilinen düşük yoğunluklu lipoprotein kolesterolün (LDL-C) kandaki düzeyinin artması ve iyi kolesterol olarak bilinen yüksek yoğunluklu lipoprotein kolesterolün (HDL-C) düzeyinin ise azalması gibi lipit metabolizma bozuklukları (dislipidemi) ile karakterize olduğu birçok çalışmada gösterilmiştir. Çeşitli epidemiyolojik çalışmalarda Tip II diyabetli (T2D) hastaların ateroskleroz ve Koroner Arter Hastalığı (KAH) komplikasyonları geliştirme riskinin daha yüksek olduğu belirtilmiştir. Çinko parmak motif transkripsiyon faktörü ailesinin üyesi olan Kruppel benzeri faktörler (KLF) normal biyolojik süreçlerde ve patolojik durumlarda gerekli olan genlerin aktivitesini düzenlemektedirler. Yapılan çalışmalarda KLF14’ün aterosklerotik KVH’da önemli rolü olduğu gösterilmiştir. Bu derlemede KLF14’ün ateroskleroz patofizyolojisindeki rolüne değinilecektir.

Keywords

Ateroskleroz, Kruppel benzeri faktör 14, Dislipidemi, Obezite, Diyabet

References

1. Değirmenci U. Koroner Arter Hastalıklarında Kruppel Benzeri Faktör 2 gen varyasyonlarının araştırılması (Doktora Tezi), Serap Yalın, Mersin, 2019.
2. Khera AV, Kathiresan S. Genetics of coronary artery disease: discovery, biology and clinical translation. Nat Rev Genet 2017;18(6): 331-344.
3. Charakida M, Tousoulis D, Stefanadis C. Early atherosclerosis in childhood: diagnostic approaches and therapeutic strategies. Int J Cardiol 2006;109(2):152-159.
4. Waqar AB, Koike T, Yu Y, Inoue T, Aoki T, Liu E, Fan J. High-fat diet without excess calories induces metabolic disorders and enhances atherosclerosis rabbits. Atherosclerosis 2010;213(1):148-155.
5. Wei X, Yang R, Wang C, Jian X, Li L, Liu H, Yang G, Li Z. A novel role forthe Kruppel-like factor 14 on macrophage inflammatory response and atherosclerosis development. Cardiovasc Pathol 2017; 27: 1-8.
6. Sarmento OF, Svingen PA, Xiong Y, Xavier RJ, McGovern D, Smryk TC, Papadakis KA, Urrutia RA, Faubion WA. A novel role for KLF14 in T regulatory cell differentiation. Cell Mol Gastroenterol Hepatol 2015; 1(2): 188-202.
7. Teslovich TM, Musunuru K, Smith AV, et al. Biological, clinical and population relevance of 95 loci for blood lipids. Nature 2010; 466 (7307): 707-713.
8. Anunciado-Koza RP, Manuel J, Koza RA. Molecular correlates of fat mass expansion in C57BL/6J mice after short-term exposure to dietary fat. Ann N Y Acad Sci2016; 1363: 50-58.
9. Koza RA, Nikonova L, Hogan J, et al. Changes in gene expression foreshadow diet-induced obesity ingenetically identical mice. PLoS Genet2006; 2(5):81.
10. Yang M, Ren Y, Lin Z, et al. Kruppel-like factor 14 increases insulin sensitivity through activation of PI3K/Akt signal pathway. Cell Signal 2015; 27(11): 2201-2208.
11. Civelek M, Lusis AJ. Conducting the metabolic syndrome orchestra. Nat Genet 2011; 43(6): 506-508.
12. Huang P, Yin RX, Huang KK, et al. Association of the KLF14 rs4731702 SNP and serum lipid levels in the Guangxi Mulao and Han populations. Biomed Res Int 2013; 2013: 231515.
13. Tanrıverdi B, Savaş TŞ. Aterosklerozun patofizyolojisi ve risk faktörleri. Marmara Pharmaceutical Journal 2017; 21: 1-9.
14. Özcan N. Koroner Kalp Hastalıkları. Kişisel Yayın: Ankara, 1997; s31-58.
15. Seidman MA, Mitchell RN, Stone JR. Pathophysiology of Atherosclerosis. Willis MS, Homeister JW, Stone JR (editors). Cellular And Molecular Pathobiology Of Cardiovascular Disease. Kindle Edition, San Diego: Elsevier Inc., 2014: 221-237.
16. Libby P, Ridker PM, Maseri A. Inflammation and atherosclerosis. Circulation 2002; 105: 1135-1143.
17. Falk E, Fuster V. Atherogenesis and its Determinants. In: Fuster V, Alexander RW, O‟ Rourke RA, Hurst‟s The Heart. 10th ed. USA. International Edition McGraw-HillMedical Publishing Division; 2000; 35: 1065-1093.
18. Andrassy M, Volz HC, Schuessler A, Gitsioudis G, Hofmann N, Laohachewin D, et al. HMGB1 is associated with atherosclerotic plaque composition and burden in patients with stable coronary artery disease. PLoS One 2012; 7: 52081.
19. Davies MJ. Atlas of Coronary Artery Disease, atherosclerosis. Lippincott Raven Publishers 1998.
20. Preiss A, Rosenberg UB, Kienlin A, et al. Molecular genetics of Kruppel, a gene required for segmentation of the Drosophila embryo. Nature 1985; 313:27–32.
21. Bieker JJ. Kruppel-like factors: three fingers in many pies. J Biol Chem2001;276:34355–34358.
22. Bieker JJ. Isolation, genomic structure, and expression of human erythroid Kruppel-like factor (EKLF). DNA Cell Biol 1996;15:347–352.
23. Turner J, Crossley M. Basic Kruppel-like factor functions within a network of interacting haematopoietic transcription factors. Int J Biochem Cell Biol 1999;31:1169–1174.
24. Scohy S, Gabant P, Van Reeth T, et al. Identification of KLF13 and KLF14 (SP6), novel members of the SP/XKLF transcription factor family. Genomics 2000; 70(1):93-101.
25. McConnell BB, Yang VW. Mammalian Kruppel like factors in health and diseases. Physiol Rev2010;90(4):1337–1381.
26. Hu W, Lu H, Zhang J, et al. Krüppel-like factor 14, a coronary artery disease associated transcription factor, inhibits endothelial inflammation via NF-κB signaling pathway. Atherosclerosis 2018; 78: 39-48.
27. Liu T, Zhang L, Joo D, Sun SC. NF-κB signaling in inflammation. Signal Transduct Target Ther 2017; 2: 17023.
28. Xie W, Li L, Zheng XL, Yin WD, Tang CK. The role of Krüppel-like factor 14 in the pathogenesis of atherosclerosis. Atherosclerosis 2017;263: 352-360.
29. Khera AV, Demler OV, Adelman SJ, et al. Cholesterol efflux capacity, HDL particle number, and incident cardiovascular events. An analysis from the jupiter trial (justification for the use of statins in prevention: an intervention trial evaluating rosuvastatin). Circulation2017; 135(25): 2494-2504.
30. Sattler K, Gräler M, Keul P, et al. Defects of high-density lipoproteins in coronary artery disease caused by low sphingosine-1-phosphate content: correction by sphingosine1-phosphate-loading. J Am Coll Cardiol2015; 66(13): 1470-1485.
31. Guo Y, Fan Y, Zhang J, et al. Perhexiline activates KLF14 and reduces therosclerosis by modulating ApoA-I production. J Clin Invest 2015; 125(10): 3819-3830.
32. Rosenson RS1, Davidson MH2, Hirsh BJ3, Kathiresan S4, Gaudet D.Genetics and causality of triglyceride-rich lipoproteins in atherosclerotic cardiovascular disease. J Am Coll Cardiol2014; 64(23): 2525-2540.
33. Kong X, Zhang X, Xing X, Zhang B, Hong J, Yang W.The association of type 2 diabetes loci identified in genome-wide association studies with metabolic syndrome and its components in a Chinese population with type 2 diabetes. PLoS One2015; 10(11): 143607.
34. Small KS, Hedman AK, Grundberg E, et al. Identification of an imprinted master trans regulator at the KLF14 locus related to multiple metabolic phenotypes. Nat Genet 2011; 43(6): 561-564.
35. Voight BF, Scott LJ, Steinthorsdottir V, et al. Twelve type 2 diabetes susceptibility loci identified through large-scale association analysis. Nat Genet2010; 42(7): 579-589.
36. Kananen L, Marttila S, Nevalainen T, et al. Aging-associated DNA methylation changes in middle-aged individuals: The Young Finns study. BMC Genomics2016; 17: 103.
37. Bacos K, Gillberg L, Volkov P, et al. Blood-based biomarkers of age-associated epigenetic changes in human islets associate with insulin secretion and diabetes. Nat Commun 2016; 7: 11089.
38. Nair AK, Piaggi P, McLean NA, et al. Assessment of established HDL-C loci for association with HDL-C levels and type 2 diabetes in Pima Indians. Diabetologia2016; 59(3):481-491.
39. Elouej S, Rejeb I, Attaoua R, et al. Gender-specific associations of genetic variants with metabolic syndrome components in the Tunisian population. Endocr Res 2016; 41(4): 300-309.
40. Glass CK, Witztum JL.Atherosclerosis. The road ahead. Cell2001; 104(4):503-516.
41. Wang J, Zhang J, Shen J, et al. Association of KCNQ1 and KLF14 polymorphisms and risk of type 2 diabetes mellitus: a global meta-analysis. Hum Immunol2014; 75(4): 342-347.
42. Fryirs MA, Barter PJ, Appavoo M, et al. Effects of high-density lipoproteins on pancreatic beta-cell insulin secretion.Arterioscler Thromb Vasc Biol2010; 30(8): 1642-1648.
43. Drew BG, Rye KA, Duffy SJ, Barter P, Kingwell BA. The emerging role of HDL in glucose metabolism. Nat Rev Endocrinol 2012; 8(4): 237-245.

The role of Kruppel-Like Factor 14 in the pathophysiology of atherosclerosis

Year 2020, Volume: 13 Issue: 2, 241 - 248, 26.08.2020

Ulaş Değirmenci Metin Yıldırım Serap Yalın

https://doi.org/10.26559/mersinsbd.675368

Abstract

Cardiovascular diseases (CVD) are responsible for one third of deaths worldwide. The common pathological condition seen in these diseases is atherosclerosis. Atherosclerosis is characterized as an inflammatory disease due to endothelial cell activation / dysfunction in its early stages.It has been shown in many studies that atherosclerosis pathology is characterized by lipid metabolism disorders (dyslipidemia), such as increased levels of low-density lipoprotein cholesterol (LDL-C) known as bad cholesterol and decreased levels of high-density lipoprotein cholesterol (HDL-C) known as good cholesterol. Various epidemiological studies have reported that patients with Type II diabetes (T2D) have a higher risk of developing complications of atherosclerosis and Coronary Artery Disease (CAD). Kruppel-like factors (KLF), a member of the zinc-finger motif transcription factor family, regulate the activity of genes required in normal biological processes and pathological conditions. KLF 14 has been shown to play an important role in atherosclerotic CVDs. In this review, the role of KLF14 in the pathophysiology of atherosclerosis will be discussed.

Keywords

Atherosclerosis, Kruppel-like Factor 14, dyslipidemia, obesity

References

1. Değirmenci U. Koroner Arter Hastalıklarında Kruppel Benzeri Faktör 2 gen varyasyonlarının araştırılması (Doktora Tezi), Serap Yalın, Mersin, 2019.
2. Khera AV, Kathiresan S. Genetics of coronary artery disease: discovery, biology and clinical translation. Nat Rev Genet 2017;18(6): 331-344.
3. Charakida M, Tousoulis D, Stefanadis C. Early atherosclerosis in childhood: diagnostic approaches and therapeutic strategies. Int J Cardiol 2006;109(2):152-159.
4. Waqar AB, Koike T, Yu Y, Inoue T, Aoki T, Liu E, Fan J. High-fat diet without excess calories induces metabolic disorders and enhances atherosclerosis rabbits. Atherosclerosis 2010;213(1):148-155.
5. Wei X, Yang R, Wang C, Jian X, Li L, Liu H, Yang G, Li Z. A novel role forthe Kruppel-like factor 14 on macrophage inflammatory response and atherosclerosis development. Cardiovasc Pathol 2017; 27: 1-8.
6. Sarmento OF, Svingen PA, Xiong Y, Xavier RJ, McGovern D, Smryk TC, Papadakis KA, Urrutia RA, Faubion WA. A novel role for KLF14 in T regulatory cell differentiation. Cell Mol Gastroenterol Hepatol 2015; 1(2): 188-202.
7. Teslovich TM, Musunuru K, Smith AV, et al. Biological, clinical and population relevance of 95 loci for blood lipids. Nature 2010; 466 (7307): 707-713.
8. Anunciado-Koza RP, Manuel J, Koza RA. Molecular correlates of fat mass expansion in C57BL/6J mice after short-term exposure to dietary fat. Ann N Y Acad Sci2016; 1363: 50-58.
9. Koza RA, Nikonova L, Hogan J, et al. Changes in gene expression foreshadow diet-induced obesity ingenetically identical mice. PLoS Genet2006; 2(5):81.
10. Yang M, Ren Y, Lin Z, et al. Kruppel-like factor 14 increases insulin sensitivity through activation of PI3K/Akt signal pathway. Cell Signal 2015; 27(11): 2201-2208.
11. Civelek M, Lusis AJ. Conducting the metabolic syndrome orchestra. Nat Genet 2011; 43(6): 506-508.
12. Huang P, Yin RX, Huang KK, et al. Association of the KLF14 rs4731702 SNP and serum lipid levels in the Guangxi Mulao and Han populations. Biomed Res Int 2013; 2013: 231515.
13. Tanrıverdi B, Savaş TŞ. Aterosklerozun patofizyolojisi ve risk faktörleri. Marmara Pharmaceutical Journal 2017; 21: 1-9.
14. Özcan N. Koroner Kalp Hastalıkları. Kişisel Yayın: Ankara, 1997; s31-58.
15. Seidman MA, Mitchell RN, Stone JR. Pathophysiology of Atherosclerosis. Willis MS, Homeister JW, Stone JR (editors). Cellular And Molecular Pathobiology Of Cardiovascular Disease. Kindle Edition, San Diego: Elsevier Inc., 2014: 221-237.
16. Libby P, Ridker PM, Maseri A. Inflammation and atherosclerosis. Circulation 2002; 105: 1135-1143.
17. Falk E, Fuster V. Atherogenesis and its Determinants. In: Fuster V, Alexander RW, O‟ Rourke RA, Hurst‟s The Heart. 10th ed. USA. International Edition McGraw-HillMedical Publishing Division; 2000; 35: 1065-1093.
18. Andrassy M, Volz HC, Schuessler A, Gitsioudis G, Hofmann N, Laohachewin D, et al. HMGB1 is associated with atherosclerotic plaque composition and burden in patients with stable coronary artery disease. PLoS One 2012; 7: 52081.
19. Davies MJ. Atlas of Coronary Artery Disease, atherosclerosis. Lippincott Raven Publishers 1998.
20. Preiss A, Rosenberg UB, Kienlin A, et al. Molecular genetics of Kruppel, a gene required for segmentation of the Drosophila embryo. Nature 1985; 313:27–32.
21. Bieker JJ. Kruppel-like factors: three fingers in many pies. J Biol Chem2001;276:34355–34358.
22. Bieker JJ. Isolation, genomic structure, and expression of human erythroid Kruppel-like factor (EKLF). DNA Cell Biol 1996;15:347–352.
23. Turner J, Crossley M. Basic Kruppel-like factor functions within a network of interacting haematopoietic transcription factors. Int J Biochem Cell Biol 1999;31:1169–1174.
24. Scohy S, Gabant P, Van Reeth T, et al. Identification of KLF13 and KLF14 (SP6), novel members of the SP/XKLF transcription factor family. Genomics 2000; 70(1):93-101.
25. McConnell BB, Yang VW. Mammalian Kruppel like factors in health and diseases. Physiol Rev2010;90(4):1337–1381.
26. Hu W, Lu H, Zhang J, et al. Krüppel-like factor 14, a coronary artery disease associated transcription factor, inhibits endothelial inflammation via NF-κB signaling pathway. Atherosclerosis 2018; 78: 39-48.
27. Liu T, Zhang L, Joo D, Sun SC. NF-κB signaling in inflammation. Signal Transduct Target Ther 2017; 2: 17023.
28. Xie W, Li L, Zheng XL, Yin WD, Tang CK. The role of Krüppel-like factor 14 in the pathogenesis of atherosclerosis. Atherosclerosis 2017;263: 352-360.
29. Khera AV, Demler OV, Adelman SJ, et al. Cholesterol efflux capacity, HDL particle number, and incident cardiovascular events. An analysis from the jupiter trial (justification for the use of statins in prevention: an intervention trial evaluating rosuvastatin). Circulation2017; 135(25): 2494-2504.
30. Sattler K, Gräler M, Keul P, et al. Defects of high-density lipoproteins in coronary artery disease caused by low sphingosine-1-phosphate content: correction by sphingosine1-phosphate-loading. J Am Coll Cardiol2015; 66(13): 1470-1485.
31. Guo Y, Fan Y, Zhang J, et al. Perhexiline activates KLF14 and reduces therosclerosis by modulating ApoA-I production. J Clin Invest 2015; 125(10): 3819-3830.
32. Rosenson RS1, Davidson MH2, Hirsh BJ3, Kathiresan S4, Gaudet D.Genetics and causality of triglyceride-rich lipoproteins in atherosclerotic cardiovascular disease. J Am Coll Cardiol2014; 64(23): 2525-2540.
33. Kong X, Zhang X, Xing X, Zhang B, Hong J, Yang W.The association of type 2 diabetes loci identified in genome-wide association studies with metabolic syndrome and its components in a Chinese population with type 2 diabetes. PLoS One2015; 10(11): 143607.
34. Small KS, Hedman AK, Grundberg E, et al. Identification of an imprinted master trans regulator at the KLF14 locus related to multiple metabolic phenotypes. Nat Genet 2011; 43(6): 561-564.
35. Voight BF, Scott LJ, Steinthorsdottir V, et al. Twelve type 2 diabetes susceptibility loci identified through large-scale association analysis. Nat Genet2010; 42(7): 579-589.
36. Kananen L, Marttila S, Nevalainen T, et al. Aging-associated DNA methylation changes in middle-aged individuals: The Young Finns study. BMC Genomics2016; 17: 103.
37. Bacos K, Gillberg L, Volkov P, et al. Blood-based biomarkers of age-associated epigenetic changes in human islets associate with insulin secretion and diabetes. Nat Commun 2016; 7: 11089.
38. Nair AK, Piaggi P, McLean NA, et al. Assessment of established HDL-C loci for association with HDL-C levels and type 2 diabetes in Pima Indians. Diabetologia2016; 59(3):481-491.
39. Elouej S, Rejeb I, Attaoua R, et al. Gender-specific associations of genetic variants with metabolic syndrome components in the Tunisian population. Endocr Res 2016; 41(4): 300-309.
40. Glass CK, Witztum JL.Atherosclerosis. The road ahead. Cell2001; 104(4):503-516.
41. Wang J, Zhang J, Shen J, et al. Association of KCNQ1 and KLF14 polymorphisms and risk of type 2 diabetes mellitus: a global meta-analysis. Hum Immunol2014; 75(4): 342-347.
42. Fryirs MA, Barter PJ, Appavoo M, et al. Effects of high-density lipoproteins on pancreatic beta-cell insulin secretion.Arterioscler Thromb Vasc Biol2010; 30(8): 1642-1648.
43. Drew BG, Rye KA, Duffy SJ, Barter P, Kingwell BA. The emerging role of HDL in glucose metabolism. Nat Rev Endocrinol 2012; 8(4): 237-245.

There are 43 citations in total.

Details

Primary Language	Turkish
Subjects	Health Care Administration
Journal Section	Articles
Authors	Ulaş Değirmenci 0000-0001-5208-6430 Metin Yıldırım 0000-0003-1346-312X Serap Yalın 0000-0002-1286-2172
Publication Date	August 26, 2020
Submission Date	January 15, 2020
Acceptance Date	March 19, 2020
Published in Issue	Year 2020 Volume: 13 Issue: 2

Cite

APA	Değirmenci, U., Yıldırım, M., & Yalın, S. (2020). Ateroskleroz patofizyolojisinde Kruppel Benzeri Faktör 14’ün rolü. Mersin Üniversitesi Sağlık Bilimleri Dergisi, 13(2), 241-248. https://doi.org/10.26559/mersinsbd.675368
AMA	Değirmenci U, Yıldırım M, Yalın S. Ateroskleroz patofizyolojisinde Kruppel Benzeri Faktör 14’ün rolü. Mersin Univ Saglık Bilim derg. August 2020;13(2):241-248. doi:10.26559/mersinsbd.675368
Chicago	Değirmenci, Ulaş, Metin Yıldırım, and Serap Yalın. “Ateroskleroz Patofizyolojisinde Kruppel Benzeri Faktör 14’ün Rolü”. Mersin Üniversitesi Sağlık Bilimleri Dergisi 13, no. 2 (August 2020): 241-48. https://doi.org/10.26559/mersinsbd.675368.
EndNote	Değirmenci U, Yıldırım M, Yalın S (August 1, 2020) Ateroskleroz patofizyolojisinde Kruppel Benzeri Faktör 14’ün rolü. Mersin Üniversitesi Sağlık Bilimleri Dergisi 13 2 241–248.
IEEE	U. Değirmenci, M. Yıldırım, and S. Yalın, “Ateroskleroz patofizyolojisinde Kruppel Benzeri Faktör 14’ün rolü”, Mersin Univ Saglık Bilim derg, vol. 13, no. 2, pp. 241–248, 2020, doi: 10.26559/mersinsbd.675368.
ISNAD	Değirmenci, Ulaş et al. “Ateroskleroz Patofizyolojisinde Kruppel Benzeri Faktör 14’ün Rolü”. Mersin Üniversitesi Sağlık Bilimleri Dergisi 13/2 (August 2020), 241-248. https://doi.org/10.26559/mersinsbd.675368.
JAMA	Değirmenci U, Yıldırım M, Yalın S. Ateroskleroz patofizyolojisinde Kruppel Benzeri Faktör 14’ün rolü. Mersin Univ Saglık Bilim derg. 2020;13:241–248.
MLA	Değirmenci, Ulaş et al. “Ateroskleroz Patofizyolojisinde Kruppel Benzeri Faktör 14’ün Rolü”. Mersin Üniversitesi Sağlık Bilimleri Dergisi, vol. 13, no. 2, 2020, pp. 241-8, doi:10.26559/mersinsbd.675368.
Vancouver	Değirmenci U, Yıldırım M, Yalın S. Ateroskleroz patofizyolojisinde Kruppel Benzeri Faktör 14’ün rolü. Mersin Univ Saglık Bilim derg. 2020;13(2):241-8.

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