HİPERGLİSEMİNİN EPİGENETİK MEKANİZMALAR İLE İLİŞKİSİ

Esma Selçuk; Didem Özkahraman; Yudi Gebri Foenna; Nilüfer Şahin Calapoğlu

doi:10.17343/sdutfd.1273169

Derleme

THE RELATİONSHİP OF HYPERGLYCEMİA WİTH EPİGENETİC MECHANİSMS

Yıl 2023, Cilt: 30 Sayı: 3, 582 - 591, 23.09.2023

Esma Selçuk Didem Özkahraman Yudi Gebri Foenna Nilüfer Şahin Calapoğlu

https://doi.org/10.17343/sdutfd.1273169

Öz

Epigenetics are traits that are inherited and reflected
in the phenotype, independent of the DNA sequence.
There is a genetic predisposition to hyperglycemia;
however, the environment plays critical roles in its
development and progress. Epigenetic changes
often translate environmental stimuli into changes in
gene expression. Epigenetic factors are mainly DNA
methylation, histone modifications and microRNAs.
Epigenetic changes, which play a role in the regulation
of all biological processes, are closely related
to diseases such as autoimmune/inflammatory,
cardiovascular, cancer, obesity and type 2 diabetes,
which are among the most important health problems
in the world and in our country. In particular, chronic
hyperglycemia, which plays a role in the pathogen of
diabetes and diabetes-related complications, affects
gene transcription through epigenetic mechanisms
such as DNA methylation, histone modifications
and microRNAs. In this review, we focused on
explaining the effects of hyperglycemia on epigenetic
mechanisms and the role of epigenetic changes it
causes in the pathogenesis of diseases.

Anahtar Kelimeler

hyperglycemia, epigenetics, complications, hyperglycemic memory, DNA methylations, histone modifications

Proje Numarası

YOK

Kaynakça

1. Villegas-Valverde CC, Kokuina E, Breff-Fonseca MC. Strengthening National Health Priorities for Diabetes Prevention and Management. MEDICC Rev. 2018;20(4):5.
2. Cugalj Kern B, Trebušak Podkrajšek K, Kovaˇc J, Šket R, Jenko Bizjan B, Tesovnik T, Debeljak M, Battelino T, Bratina N. The Role of Epigenetic Modifications in Late Complications in Type 1 Diabetes. Genes. 2022;13:705.
3. D’Urso A, Brickner J. Epigenetic transcriptional memory. Curr Genet. 2017; 63:435–439.
4. Prandi FR, Lecis D, Illuminato F, Milite M, Celotto R, Lerakis S, Romeo F, Barillà F. Epigenetic Modifications and Non-Coding RNA in Diabetes-Mellitus-Induced Coronary Artery Disease: Pathophysiological Link and New Therapeutic Frontiers. Int. J. Mol. Sci. 2022, 23, 4589.
5. Klimontov VV, Saik OV, Korbut AI. Glucose Variability: How Does It Work? Int. J. Mol. Sci. 2021;22:7783.
6. Khan RMM, Chua ZJY, Tan JC, Yang Y, Liao Z, Zhao Y. From Pre-Diabetes to Diabetes: Diagnosis, Treatments and Translational Research. Medicina. 2019;55:546.
7. Hammer M, Storey S, Hershey DS, Brady VJ, Davis E, Mandolfo N, Bryant AL, Olausson J. Hyperglycemia and Cancer: A State- of-the-Science Review. Oncol Nurs Forum. 2019;46(4):459- 472.
8. Jia G, Whaley-Connell A, R. Sowers J. Diabetic cardiomyopathy: a hyperglycaemia- and insulinresistance-induced heart diseas. Diabetologia. 2018;61(1): 21–28.
9. Kang Q, Yang C. Oxidative stress and diabetic retinopathy: Molecular mechanisms, pathogenetic role and therapeutic implications. Redox Biology. 2020;37:101799.
10. Çetiner Ö, Rakıcıoğlu N. Hiperglisemi, Oksidatif Stres ve Tip 2 Diyabette Oksidatif Stres Belirteçlerinin Tanımlanması. Oksidatif Stres ve Tip 2 Diyabette Oksidatif Stres Belirteçlerinin Tanımlanması. Türk Diyab Obez. 2020;1:60-68.
11. Venugopal S. Hyperglycemic memory and its long-term effects in diabetes. Biomed. Res. 2016;2016:S354–361.
12. Diabetes Control and Complications Trial Research Group. Effect of intensive diabetes treatment on the development and progression of long-term complications in adolescents with insulin-dependent diabetes mellitus: Diabetes Control and Complications Trial. J. Pediatr. 1994;125:177–188.
13. Testa R, Bonfigli AR, Prattichizzo F, La Sala L, De Nigris V, Ceriello A. The “Metabolic Memory” Theory and the Early Treatment of Hyperglycemia in Prevention of Diabetic Complications. Nutrients. 2017;9:437
14. Nathan DM. The diabetes control and complications trial/epidemiology of diabetes interventions and complications study at 30 years: Overview. Diabetes Care. 2014;37:9–16.
15. Franzago M, Fraticelli F, Stuppia L, Vitacolonna E. Nutrigenetics, epigenetics and gestational diabetes: consequences in mother and child. Epigenetics. 2019;14(3):215-235.
16. Tzika E, Dreker T, Imhof A. Epigenetics and Metabolism in Health and Disease. Front. Genet. 2018;9:361.
17. Singh R, Chandel S, Dey D, Ghosh A, Roy S, Ravichandiran V, Ghosh D. Epigenetic modification and therapeutic targets of diabetes mellitus. Bioscience Reports. 2020;40:BSR20202160.
18. Livingstone C, Borai A. Insulin-like growth factor-II: its role in metabolic and endocrine disease. Clin. Endocrinol. 2014;80:773– 781.
19. Sparago A, Cerrato F, Vernucci M, Ferrero GB, Silengo MC, Riccio A. Microdeletions in the human H19 DMR result in loss of IGF2 imprinting and Beckwith-Wiedemann syndrome. Nat. Genet. 2004;36:958–960.
20. Mokbel N, Hoffman NJ, Girgis CM, Small L, Turner N, Daly RJ, et al. Grb10 deletion enhances muscle cell proliferation, differentiation and GLUT4 plasma membrane translocation. J. Cell. Physiol. 2014;229:1753–1764.
21. Zhang S, Rattanatray L, McMillen IC, Suter CM, Morrison JL. Periconceptional nutrition and the early programming of a life of obesity or adversity. Prog. Biophys. Mol. Biol. 2011;106:307–314.
22. Charalambous M, Hernandez A. Genomic imprinting of the type 3 thyroid hormone deiodinase gene: regulation and developmental implications. Biochim. Biophys. Acta 2013;1830:3946–3955.
23. T. Keating S, El-Osta A. Epigenetics and Metabolism. Circ Res. 2015;116:715-736.
24. Can Mİ, Aslan A. Epigenetik Mekanizmalar ve Bazı Güncel Çalışmalar. Karaelmas Fen Müh. Derg. 2016; 6(2):445-452.
25. İmre KE, Akyol Mutlu A. Epigenetik Mekanizmalar: Maternal Makro Besin Ögesi Alımının Etkileri. Bes Diy Derg. 2022;50(1):92-100.
26. Bell CG, Teschendorff AE, Rakyan VK, Maxwell AP, Beck S, Savage DA. Genome-wide DNA methylation analysis for diabetic nephropathy in type 1 diabetes mellitus. BMC Med. Genom. 2010;3:33.
27. Brennan EP, Ehrich M, Brazil DP, Crean JK, Murphy M, Sadlier DM, Martin F, Godson C, van den Boom D, Maxwell AP, et al. DNA methylation profiling in cell models of diabetic nephropathy. Epigenetics. 2010;5:396–401.
28. Dalfrà MG, Burlina S, Del Vescovo GG, Lapolla A. Genetics and Epigenetics: New Insight on Gestational Diabetes Mellitus. Front. Endocrinol. 2020;11:602477.
29. Doğan R, Aktaş RG. Epigenetik Mekanizmalar ve Hepatosellüler Karsinoma. Maltepe Tıp Dergisi. 2016;8:3.
30. Tessarz P, Kouzarides T. Histone core modifications regulating nucleosome structure and dynamics. Nat. Rev. Mol. Cell Biol. 2014;15:703–708.
31. Bannister AJ, Kouzarides T. Regulation of chromatin by histone modifications. Cell Res. 2011;21:381–395.
32. Barnes CE, English DM, Cowley SM. Acetylation and Co: An expanding repertoire of histone acylations regulates chromatin and transcription. Essays Biochem. 2019;63:97–107.
33. Rossetto D, Avvakumov N, Côté J. Histone phosphorylation. Epigenetics. 2012;7:1098–1108.
34. Greer EL, Shi Y. Histone methylation: A dynamic mark in health, disease and inheritance. Nat. Rev. Genet. 2012;13:343–357.
35. Cao J, Yan Q. Histone ubiquitination and deubiquitination in transcription, DNA damage response, and cancer. Front. Oncol. 2012;2:1–9.
36. Cobos SN, Bennett SA, Torrente MP. The impact of histone post-translational modifications in neurodegenerative diseases. Biochim. Biophys. Acta Mol. Basis Dis. 2019;1865:1982–1991.
37. Wang Y, Yuan Q, Xie L. Histone Modifications in Aging: The Underlying Mechanisms and Implications. Curr. Stem Cell Res. Ther. 2018;13:125–135.
38. Audia JE, Campbell RM. Histone modifications and cancer. Cold Spring Harb. Perspect. Biol. 2016;8:1–31.
39. Miao F, Wu X, Zhang L, Yuan YC, Riggs AD, Natarajan R. Genome- wide analysis of histone lysine methylation variations caused by diabetic conditions in human monocytes. J. Biol. Chem. 2007;282:13854–13863.
40. Miao F, Chen Z, Genuth S, et al. Evaluating the role of epigenetic histone modifications in the metabolic memory of type 1 diabetes. Diabetes. 2014;63:1748–1762.
41. Sun G, Reddy MA, Yuan H, Lanting L, Kato M, Natarajan R. Epigenetic histone methylation modulates fibrotic gene expression.J. Am. Soc. Nephrol. 2010;21:2069–2080.
42. Li X, Li C, Li X, et al. Involvement of histone lysine methylation in p21 gene expression in rat kidney in vivo and rat mesangial cells in vitro under diabetic conditions. J. Diabetes Res. 2016;2016:3853242.
43. Chen J, Guo Y, Zeng W, et al. ER stress triggers MCP-1 expression through SET7 / 9-induced histone methylation in the kidneys of db / db mice. Am. J. Physiol. 2014;306:916–925.
44. Li Y, Reddy MA, Miao F, et al. Role of the histone H3 lysine 4 methyltransferase, SET7/9, in the regulation of NF-κB-dependent inflammatory genes: Relevance to diabetes and inflammation. J. Biol. Chem. 2008;283:26771–26781
45. Villeneuve LM, Reddy MA, et al. Epigenetic histone H3 lysine 9 methylation in metabolic memory and inflammatory phenotype of vascular smooth muscle cells in diabetes. Proc. Natl. Acad. Sci. 2008;105:9047–9052.
46. Jia Y, Reddy MA, Das S, et al. Dysregulation of histone H3 lysine 27 trimethylation in transforming growth factor-β1-induced gene expression in mesangial cells and diabetic kidney. J. Biol. Chem. 2019;294:12695–12707.
47. Lin SH, Ho WT, Wang YT, et al. Histone methyltransferase Suv39h1 attenuates high glucose-induced fibronectin and p21WAF1 in mesangial cells. Int. J. Biochem. Cell Biol. 2016;78:96–105.
48. Syreeni A, El-Osta A, Forsblom C, et al. Genetic examination of SETD7 and SUV39H1/H2 methyltransferases and the risk of diabetes complications in patients with type 1 diabetes. Diabetes. 2011; 60:3073–3080.
49. Bijkerk R, Duijs JMGJ, Khairoun M, et al. Circulating MicroRNAs associate with diabetic nephropathy and systemic microvascular damage and normalize after simultaneous pancreas-kidney transplantation. Am. J. Transplant. 2015;15:1081–1090.
50. Assmann TS, Recamonde-Mendoza M, Costa AR, et al. Circulating miRNAs in diabetic kidney disease: Case–control study and in silico analyses. Acta Diabetol. 2019;56:55–65.
51. Zampetaki A, Willeit P, Burr S, et al. Angiogenic microRNAs linked to incidence and progression of diabetic retinopathy in type 1 diabetes. Diabetes. 2016;65:216–227.
52. Santos-Bezerra DP, Santos AS, Guimarães, GC, et al. Micro-RNAs 518d-3p and 618 are upregulated in individuals with type 1 diabetes with multiple microvascular complications. Front. Endocrinol. 2019;10:385.
53. Bera A, Das F, Ghosh-Choudhury N, Mariappan MM, Kasinath BS, Choudhury GG. Reciprocal regulation of miR-214 and PTEN by high glucose regulates renal glomerular mesangial and proximal tubular epithelial cell hypertrophy and matrix expansion. Am. J. Physiol. Cell Physiol. 2017;313:C430–447.
54. Wang Q, Wang Y, Minto AW, Wang J, Shi Q, Li X, Quigg RJ. MicroRNA-377 is up-regulated and can lead to increased fibronectin production in diabetic nephropathy. FASEB J. 2008;22:4126–4135.
55. Brasacchio D, Okabe J, Tikellis C, Balcerczyk A, George P, Baker EK, El-Osta A. Hyperglycemia induces a dynamic cooperativity of histone methylase and demethylase enzymes associated with gene-activating epigenetic marks that coexist on the lysine tail. Diabetes. 2009;58(5):1229-1236.
56. El-Osta A, Brasacchio D, Yao D, Pocai A, Jones PL, Roeder RG, Brownlee M. Transient high glucose causes persistent epigenetic changes and altered gene expression during subsequent normoglycemia. The Journal of experimental medicine. 2008;205(10):2409-2417.
57. Takizawa F, Mizutani S, Ogawa Y, Sawada N. Glucose-independent persistence of PAI-1 gene expression and H3K4 tri-methylation in type 1 diabetic mouse endothelium: implication in metabolic memory. Biochemical and biophysical research communications. 2013;433(1):66-72.
58. Gialitakis M, Arampatzi P, Makatounakis T, Papamatheakis J. Gamma interferon-dependent transcriptional memory via relocalization of a gene locus to PML nuclear bodies. Molecular and cellular biology. 2010;30(8):2046-2056.
59. Crisp PA, Ganguly D, Eichten SR, Borevitz JO, Pogson BJ. Reconsidering plant memory: Intersections between stress recovery, RNA turnover, and epigenetics. Science advances. 2016;2(2):e1501340.
60. Davison GW, Irwin RE, Walsh CP. The metabolic-epigenetic nexus in type 2 diabetes mellitus. Free Radical Biology and Medicine. 202;170:194-206.
61. Rutter GA, Georgiadou E, Martinez-Sanchez A, Pullen TJ. Metabolic and functional specialisations of the pancreatic beta cell: gene disallowance, mitochondrial metabolism and intercellular connectivity. Diabetologia. 2020;63:1990-1998.
62. Rönn T, Ling C. DNA methylation as a diagnostic and therapeutic target in the battle against Type 2 diabetes. Epigenomics. 2015;7(3):451-460.

HİPERGLİSEMİNİN EPİGENETİK MEKANİZMALAR İLE İLİŞKİSİ

Yıl 2023, Cilt: 30 Sayı: 3, 582 - 591, 23.09.2023

Esma Selçuk Didem Özkahraman Yudi Gebri Foenna Nilüfer Şahin Calapoğlu

https://doi.org/10.17343/sdutfd.1273169

Öz

Epigenetik, DNA dizisinden bağımsız olarak fenotipe
yansıyan ve kalıtsal olarak aktarılabilen özelliklerdir.
Hiperglisemide genetik yatkınlık söz konusudur; ancak
çevre, gelişmesinde ve ilerlemesinde kritik roller
oynar. Epigenetik değişiklikler genellikle çevresel uyaranları
gen ifadesindeki değişikliklere çevirir. Epigenetik
faktörler, temel olarak DNA metilasyonu, histon
modifikasyonları ve mikroRNA'lardır. Tüm biyolojik
süreçlerin düzenlenmesinde rol oynayan epigenetik
değişiklikler, otoimmüne/inflamatuar, kardiyovasküler,
kanser, obezite ve tip 2 diyabet gibi tüm dünyada ve
ülkemizde önemli sağlık sorunlarının başında gelen
hastalıklar ile de yakından ilişkilidir. Özellikle diyabet
ve diyabetle ilişkili komplikasyonların patojeninizde rol
oynayan kronik hiperglisemi, DNA metilasyonu, histon
modifikasyonları ve mikro RNA’lar gibi epigenetik
mekanizmalar aracılığıyla gen transkripsiyonunu etkilemektedir.
Bu derlemede, hipergliseminin, epigenetik
mekanizmalar üzerindeki etkilerine ve yol açtığı epigenetik
değişimlerin hastalıklarların patogenezindeki
rollerini açıklamaya odaklandık.

Anahtar Kelimeler

hiperglisemi, epigenetik, komplikasyonlar, hiperglisemik hafıza, DNA metilasyonları, histon modifikasyonları

Destekleyen Kurum

YOK

Proje Numarası

YOK

Teşekkür

Bu çalışmada emeği geçen, değerli hocamız Prof. Dr. Mustafa CALAPOĞLU'na teşekkür ederiz.

Kaynakça

1. Villegas-Valverde CC, Kokuina E, Breff-Fonseca MC. Strengthening National Health Priorities for Diabetes Prevention and Management. MEDICC Rev. 2018;20(4):5.
2. Cugalj Kern B, Trebušak Podkrajšek K, Kovaˇc J, Šket R, Jenko Bizjan B, Tesovnik T, Debeljak M, Battelino T, Bratina N. The Role of Epigenetic Modifications in Late Complications in Type 1 Diabetes. Genes. 2022;13:705.
3. D’Urso A, Brickner J. Epigenetic transcriptional memory. Curr Genet. 2017; 63:435–439.
4. Prandi FR, Lecis D, Illuminato F, Milite M, Celotto R, Lerakis S, Romeo F, Barillà F. Epigenetic Modifications and Non-Coding RNA in Diabetes-Mellitus-Induced Coronary Artery Disease: Pathophysiological Link and New Therapeutic Frontiers. Int. J. Mol. Sci. 2022, 23, 4589.
5. Klimontov VV, Saik OV, Korbut AI. Glucose Variability: How Does It Work? Int. J. Mol. Sci. 2021;22:7783.
6. Khan RMM, Chua ZJY, Tan JC, Yang Y, Liao Z, Zhao Y. From Pre-Diabetes to Diabetes: Diagnosis, Treatments and Translational Research. Medicina. 2019;55:546.
7. Hammer M, Storey S, Hershey DS, Brady VJ, Davis E, Mandolfo N, Bryant AL, Olausson J. Hyperglycemia and Cancer: A State- of-the-Science Review. Oncol Nurs Forum. 2019;46(4):459- 472.
8. Jia G, Whaley-Connell A, R. Sowers J. Diabetic cardiomyopathy: a hyperglycaemia- and insulinresistance-induced heart diseas. Diabetologia. 2018;61(1): 21–28.
9. Kang Q, Yang C. Oxidative stress and diabetic retinopathy: Molecular mechanisms, pathogenetic role and therapeutic implications. Redox Biology. 2020;37:101799.
10. Çetiner Ö, Rakıcıoğlu N. Hiperglisemi, Oksidatif Stres ve Tip 2 Diyabette Oksidatif Stres Belirteçlerinin Tanımlanması. Oksidatif Stres ve Tip 2 Diyabette Oksidatif Stres Belirteçlerinin Tanımlanması. Türk Diyab Obez. 2020;1:60-68.
11. Venugopal S. Hyperglycemic memory and its long-term effects in diabetes. Biomed. Res. 2016;2016:S354–361.
12. Diabetes Control and Complications Trial Research Group. Effect of intensive diabetes treatment on the development and progression of long-term complications in adolescents with insulin-dependent diabetes mellitus: Diabetes Control and Complications Trial. J. Pediatr. 1994;125:177–188.
13. Testa R, Bonfigli AR, Prattichizzo F, La Sala L, De Nigris V, Ceriello A. The “Metabolic Memory” Theory and the Early Treatment of Hyperglycemia in Prevention of Diabetic Complications. Nutrients. 2017;9:437
14. Nathan DM. The diabetes control and complications trial/epidemiology of diabetes interventions and complications study at 30 years: Overview. Diabetes Care. 2014;37:9–16.
15. Franzago M, Fraticelli F, Stuppia L, Vitacolonna E. Nutrigenetics, epigenetics and gestational diabetes: consequences in mother and child. Epigenetics. 2019;14(3):215-235.
16. Tzika E, Dreker T, Imhof A. Epigenetics and Metabolism in Health and Disease. Front. Genet. 2018;9:361.
17. Singh R, Chandel S, Dey D, Ghosh A, Roy S, Ravichandiran V, Ghosh D. Epigenetic modification and therapeutic targets of diabetes mellitus. Bioscience Reports. 2020;40:BSR20202160.
18. Livingstone C, Borai A. Insulin-like growth factor-II: its role in metabolic and endocrine disease. Clin. Endocrinol. 2014;80:773– 781.
19. Sparago A, Cerrato F, Vernucci M, Ferrero GB, Silengo MC, Riccio A. Microdeletions in the human H19 DMR result in loss of IGF2 imprinting and Beckwith-Wiedemann syndrome. Nat. Genet. 2004;36:958–960.
20. Mokbel N, Hoffman NJ, Girgis CM, Small L, Turner N, Daly RJ, et al. Grb10 deletion enhances muscle cell proliferation, differentiation and GLUT4 plasma membrane translocation. J. Cell. Physiol. 2014;229:1753–1764.
21. Zhang S, Rattanatray L, McMillen IC, Suter CM, Morrison JL. Periconceptional nutrition and the early programming of a life of obesity or adversity. Prog. Biophys. Mol. Biol. 2011;106:307–314.
22. Charalambous M, Hernandez A. Genomic imprinting of the type 3 thyroid hormone deiodinase gene: regulation and developmental implications. Biochim. Biophys. Acta 2013;1830:3946–3955.
23. T. Keating S, El-Osta A. Epigenetics and Metabolism. Circ Res. 2015;116:715-736.
24. Can Mİ, Aslan A. Epigenetik Mekanizmalar ve Bazı Güncel Çalışmalar. Karaelmas Fen Müh. Derg. 2016; 6(2):445-452.
25. İmre KE, Akyol Mutlu A. Epigenetik Mekanizmalar: Maternal Makro Besin Ögesi Alımının Etkileri. Bes Diy Derg. 2022;50(1):92-100.
26. Bell CG, Teschendorff AE, Rakyan VK, Maxwell AP, Beck S, Savage DA. Genome-wide DNA methylation analysis for diabetic nephropathy in type 1 diabetes mellitus. BMC Med. Genom. 2010;3:33.
27. Brennan EP, Ehrich M, Brazil DP, Crean JK, Murphy M, Sadlier DM, Martin F, Godson C, van den Boom D, Maxwell AP, et al. DNA methylation profiling in cell models of diabetic nephropathy. Epigenetics. 2010;5:396–401.
28. Dalfrà MG, Burlina S, Del Vescovo GG, Lapolla A. Genetics and Epigenetics: New Insight on Gestational Diabetes Mellitus. Front. Endocrinol. 2020;11:602477.
29. Doğan R, Aktaş RG. Epigenetik Mekanizmalar ve Hepatosellüler Karsinoma. Maltepe Tıp Dergisi. 2016;8:3.
30. Tessarz P, Kouzarides T. Histone core modifications regulating nucleosome structure and dynamics. Nat. Rev. Mol. Cell Biol. 2014;15:703–708.
31. Bannister AJ, Kouzarides T. Regulation of chromatin by histone modifications. Cell Res. 2011;21:381–395.
32. Barnes CE, English DM, Cowley SM. Acetylation and Co: An expanding repertoire of histone acylations regulates chromatin and transcription. Essays Biochem. 2019;63:97–107.
33. Rossetto D, Avvakumov N, Côté J. Histone phosphorylation. Epigenetics. 2012;7:1098–1108.
34. Greer EL, Shi Y. Histone methylation: A dynamic mark in health, disease and inheritance. Nat. Rev. Genet. 2012;13:343–357.
35. Cao J, Yan Q. Histone ubiquitination and deubiquitination in transcription, DNA damage response, and cancer. Front. Oncol. 2012;2:1–9.
36. Cobos SN, Bennett SA, Torrente MP. The impact of histone post-translational modifications in neurodegenerative diseases. Biochim. Biophys. Acta Mol. Basis Dis. 2019;1865:1982–1991.
37. Wang Y, Yuan Q, Xie L. Histone Modifications in Aging: The Underlying Mechanisms and Implications. Curr. Stem Cell Res. Ther. 2018;13:125–135.
38. Audia JE, Campbell RM. Histone modifications and cancer. Cold Spring Harb. Perspect. Biol. 2016;8:1–31.
39. Miao F, Wu X, Zhang L, Yuan YC, Riggs AD, Natarajan R. Genome- wide analysis of histone lysine methylation variations caused by diabetic conditions in human monocytes. J. Biol. Chem. 2007;282:13854–13863.
40. Miao F, Chen Z, Genuth S, et al. Evaluating the role of epigenetic histone modifications in the metabolic memory of type 1 diabetes. Diabetes. 2014;63:1748–1762.
41. Sun G, Reddy MA, Yuan H, Lanting L, Kato M, Natarajan R. Epigenetic histone methylation modulates fibrotic gene expression.J. Am. Soc. Nephrol. 2010;21:2069–2080.
42. Li X, Li C, Li X, et al. Involvement of histone lysine methylation in p21 gene expression in rat kidney in vivo and rat mesangial cells in vitro under diabetic conditions. J. Diabetes Res. 2016;2016:3853242.
43. Chen J, Guo Y, Zeng W, et al. ER stress triggers MCP-1 expression through SET7 / 9-induced histone methylation in the kidneys of db / db mice. Am. J. Physiol. 2014;306:916–925.
44. Li Y, Reddy MA, Miao F, et al. Role of the histone H3 lysine 4 methyltransferase, SET7/9, in the regulation of NF-κB-dependent inflammatory genes: Relevance to diabetes and inflammation. J. Biol. Chem. 2008;283:26771–26781
45. Villeneuve LM, Reddy MA, et al. Epigenetic histone H3 lysine 9 methylation in metabolic memory and inflammatory phenotype of vascular smooth muscle cells in diabetes. Proc. Natl. Acad. Sci. 2008;105:9047–9052.
46. Jia Y, Reddy MA, Das S, et al. Dysregulation of histone H3 lysine 27 trimethylation in transforming growth factor-β1-induced gene expression in mesangial cells and diabetic kidney. J. Biol. Chem. 2019;294:12695–12707.
47. Lin SH, Ho WT, Wang YT, et al. Histone methyltransferase Suv39h1 attenuates high glucose-induced fibronectin and p21WAF1 in mesangial cells. Int. J. Biochem. Cell Biol. 2016;78:96–105.
48. Syreeni A, El-Osta A, Forsblom C, et al. Genetic examination of SETD7 and SUV39H1/H2 methyltransferases and the risk of diabetes complications in patients with type 1 diabetes. Diabetes. 2011; 60:3073–3080.
49. Bijkerk R, Duijs JMGJ, Khairoun M, et al. Circulating MicroRNAs associate with diabetic nephropathy and systemic microvascular damage and normalize after simultaneous pancreas-kidney transplantation. Am. J. Transplant. 2015;15:1081–1090.
50. Assmann TS, Recamonde-Mendoza M, Costa AR, et al. Circulating miRNAs in diabetic kidney disease: Case–control study and in silico analyses. Acta Diabetol. 2019;56:55–65.
51. Zampetaki A, Willeit P, Burr S, et al. Angiogenic microRNAs linked to incidence and progression of diabetic retinopathy in type 1 diabetes. Diabetes. 2016;65:216–227.
52. Santos-Bezerra DP, Santos AS, Guimarães, GC, et al. Micro-RNAs 518d-3p and 618 are upregulated in individuals with type 1 diabetes with multiple microvascular complications. Front. Endocrinol. 2019;10:385.
53. Bera A, Das F, Ghosh-Choudhury N, Mariappan MM, Kasinath BS, Choudhury GG. Reciprocal regulation of miR-214 and PTEN by high glucose regulates renal glomerular mesangial and proximal tubular epithelial cell hypertrophy and matrix expansion. Am. J. Physiol. Cell Physiol. 2017;313:C430–447.
54. Wang Q, Wang Y, Minto AW, Wang J, Shi Q, Li X, Quigg RJ. MicroRNA-377 is up-regulated and can lead to increased fibronectin production in diabetic nephropathy. FASEB J. 2008;22:4126–4135.
55. Brasacchio D, Okabe J, Tikellis C, Balcerczyk A, George P, Baker EK, El-Osta A. Hyperglycemia induces a dynamic cooperativity of histone methylase and demethylase enzymes associated with gene-activating epigenetic marks that coexist on the lysine tail. Diabetes. 2009;58(5):1229-1236.
56. El-Osta A, Brasacchio D, Yao D, Pocai A, Jones PL, Roeder RG, Brownlee M. Transient high glucose causes persistent epigenetic changes and altered gene expression during subsequent normoglycemia. The Journal of experimental medicine. 2008;205(10):2409-2417.
57. Takizawa F, Mizutani S, Ogawa Y, Sawada N. Glucose-independent persistence of PAI-1 gene expression and H3K4 tri-methylation in type 1 diabetic mouse endothelium: implication in metabolic memory. Biochemical and biophysical research communications. 2013;433(1):66-72.
58. Gialitakis M, Arampatzi P, Makatounakis T, Papamatheakis J. Gamma interferon-dependent transcriptional memory via relocalization of a gene locus to PML nuclear bodies. Molecular and cellular biology. 2010;30(8):2046-2056.
59. Crisp PA, Ganguly D, Eichten SR, Borevitz JO, Pogson BJ. Reconsidering plant memory: Intersections between stress recovery, RNA turnover, and epigenetics. Science advances. 2016;2(2):e1501340.
60. Davison GW, Irwin RE, Walsh CP. The metabolic-epigenetic nexus in type 2 diabetes mellitus. Free Radical Biology and Medicine. 202;170:194-206.
61. Rutter GA, Georgiadou E, Martinez-Sanchez A, Pullen TJ. Metabolic and functional specialisations of the pancreatic beta cell: gene disallowance, mitochondrial metabolism and intercellular connectivity. Diabetologia. 2020;63:1990-1998.
62. Rönn T, Ling C. DNA methylation as a diagnostic and therapeutic target in the battle against Type 2 diabetes. Epigenomics. 2015;7(3):451-460.

Toplam 62 adet kaynakça vardır.

Ayrıntılar

Birincil Dil	Türkçe
Konular	Klinik Tıp Bilimleri
Bölüm	Derlemeler
Yazarlar	Esma Selçuk 0000-0002-1481-7834 Didem Özkahraman 0000-0002-3951-0740 Yudi Gebri Foenna 0000-0002-1380-7191 Nilüfer Şahin Calapoğlu 0000-0002-7376-1607
Proje Numarası	YOK
Yayımlanma Tarihi	23 Eylül 2023
Gönderilme Tarihi	29 Mart 2023
Kabul Tarihi	20 Haziran 2023
Yayımlandığı Sayı	Yıl 2023 Cilt: 30 Sayı: 3

Kaynak Göster

Vancouver	Selçuk E, Özkahraman D, Foenna YG, Şahin Calapoğlu N. HİPERGLİSEMİNİN EPİGENETİK MEKANİZMALAR İLE İLİŞKİSİ. SDÜ Tıp Fak Derg. 2023;30(3):582-91.

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Süleyman Demirel Üniversitesi Tıp Fakültesi Dergisi/Medical Journal of Süleyman Demirel University is licensed under Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International.