Файл: Изучение молекулярных предикторов сосудистого риска опосредованного эндотелиальной дисфункцией у людей с сахарным диабетом 2 типа.docx

ВУЗ: Не указан

Категория: Не указан

Дисциплина: Не указана

Добавлен: 05.12.2023

Просмотров: 123

Скачиваний: 1

ВНИМАНИЕ! Если данный файл нарушает Ваши авторские права, то обязательно сообщите нам.


↑18. Derham BK, Harding JJ. Effects of modifications of alpha-crystallin on its chaperone and other properties. Biochem J. 2002;364(Pt 3):711-717. https://doi.org/10.1042/BJ20011512

↑19. Choi JH, Banks AS, Estall JL, et al. Anti-diabetic drugs inhibit obesity-linked phosphorylation of PPARgamma by Cdk5. Nature. 2010;466(7305):451-456. https://doi.org/10.1038/nature09291

↑20. Oriente F, Fernandez Diaz LC, Miele C, et al. Prep1 deficiency induces protection from diabetes and increased insulin sensitivity through a p160-mediated mechanism. Mol Cell Biol. 2008;28(18):5634-5645. https://doi.org/10.1128/MCB.00117-08

↑21. Oriente F, Cabaro S, Liotti A, et al. PREP1 deficiency downregulates hepatic lipogenesis and attenuates steatohepatitis in mice. Diabetologia. 2013;56(12):2713-2722. https://doi.org/10.1007/s00125-013-3053-3

↑22. Penkov DN, Egorov AD, Mozgovaya MN, Tkachuk VA. Insulin resistance and adipogenesis: role of transcription and secreted factors. Biochemistry (Mosc). 2013;78(1):8-18. https://doi.org/10.1134/S0006297913010021

↑23. Erickson HP. Irisin and FNDC5 in retrospect: An exercise hormone or a transmembrane receptor? Adipocyte. 2013;2(4):289-293. https://doi.org/10.4161/adip.26082

↑24. Bostrom P, Wu J, Jedrychowski MP, et al. A PGC1-alpha-dependent myokine that drives brown-fat-like development of white fat and thermogenesis. Nature. 2012;481(7382):463-468. https://doi.org/10.1038/nature10777

↑25. Nedergaard J, Wang Y, Cannon B. Cell proliferation and apoptosis inhibition: essential processes for recruitment of the full thermogenic capacity of brown adipose tissue. Biochim Biophys Acta Mol Cell Biol Lipids. 2018. https://doi.org/10.1016/j.bbalip.2018.06.013

↑26. Lidell ME, Betz MJ, Enerback S. Brown adipose tissue and its therapeutic potential. J Intern Med. 2014;276(4):364-377. https://doi.org/10.1111/joim.12255

↑27. Sidossis L, Kajimura S. Brown and beige fat in humans: thermogenic adipocytes that control energy and glucose homeostasis. J Clin Invest. 2015;125(2):478-486. https://doi.org/10.1172/JCI78362

↑28. Wu J, Bostrom P, Sparks LM, et al. Beige adipocytes are a distinct type of thermogenic fat cell in mouse and human. Cell. 2012;150(2):366-376. https://doi.org/10.1016/j.cell.2012.05.016

↑29. Giralt M, Villarroya F. White, brown, beige/brite: different adipose cells for different functions? Endocrinology. 2013;154(9):2992-3000. https://doi.org/10.1210/en.2013-1403

↑30. Carobbio S, Guenantin AC, Samuelson I, et al. Brown and beige fat: From molecules to physiology and pathophysiology. Biochim Biophys Acta Mol Cell Biol Lipids. 2018. https://doi.org/10.1016/j.bbalip.2018.05.013

↑31. Cypess AM, Lehman S, Williams G, et al. Identification and importance of brown adipose tissue in adult humans. N Engl J Med. 2009;360(15):1509-1517. https://doi.org/10.1056/NEJMoa0810780

↑32. Cypess AM, Haft CR, Laughlin MR, Hu HH. Brown fat in humans: consensus points and experimental guidelines. Cell Metab. 2014;20(3):408-415. https://doi.org/10.1016/j.cmet.2014.07.025

↑33. Hany TF, Steinert HC, Goerres GW, et al. PET diagnostic accuracy: improvement with in-line PET-CT system: initial results. Radiology. 2002;225(2):575-581. https://doi.org/10.1148/radiol.2252011568

↑34. Karlas A, Reber J, Liapis E, et al. Multispectral Optoacoustic Tomography of Brown Adipose Tissue. Handb Exp Pharmacol. 2018. https://doi.org/10.1007/164_2018_141

↑35. Groop LC, Widén E, Ferrannini E. Insulin resistance and insulin deficiency in the pathogenesis of Type 2 (non-insulin-dependent) diabetes mellitus: errors of metabolism or of methods? Diabetologia. 1993;36(12):1326-1331. https://doi.org/10.1007/bf00400814

↑36. Майоров А.Ю., Урбанова К.А., Галстян Г.Р. Методы количественной оценки инсулинорезистентности // Ожирение и метаболизм. -2009. -Т. 6. -№2. -С. 19-23. [Mayorov AY, Urbanova KA, Galstyan GR. Methods for guantificative assessment of insulin resistance. Obesity and metabolism. 2009;6(2):19-23. (In Russ.)] https://doi.org/10.14341/2071-8713-5313

↑37. Sorkina E, Frolova E, Rusinova D, et al. Progressive Generalized Lipodystrophy as a Manifestation of Autoimmune Polyglandular Syndrome Type 1. J Clin Endocrinol Metab. 2016;101(4):1344-1347. https://doi.org/10.1210/jc.2015-3722


↑38. Судницына М.В., Гусев И.Б. Малые белки теплового шока и диабет // Вестник Московского университета. Серия 16: Биология. -2015. -№2. -С. 24-30. [Sudnitsyna MV, Gusev NB. Small heat shock proteins and diabetes. Vestnik Moskovskogo universiteta. Seriya 16. Biologiya. 2015;(2):24-30. (In Russ.)]

↑39. Судницына М.В., Гусев Н.Б. Метилглиоксаль и малые белки теплового шока // Биохимия. -2017. -Т. 82.- №7. -С. 987-997. [Sudnitsyna MV, Gusev NB. Methylglyoxal and small heat shock proteins. Biochemistry. 2017;82(7):987-997. (In Russ.)]

↑40. Muranova LK, Perfilov MM, Serebryakova MV, Gusev NB. Effect of methylglyoxal modification on the structure and properties of human small heat shock protein HspB6 (Hsp20). Cell Stress Chaperones. 2016;21(4):617-629. https://doi.org/10.1007/s12192-016-0686-4

↑41. Sluchanko NN, Chebotareva NA, Gusev NB. Quaternary structure of human small heat shock protein HSPB6 (Hsp20) in crowded media modeled by trimethylamine N-oxide (TMAO): Effect of protein phosphorylation. Biochimie. 2015;108:68-75. https://doi.org/10.1016/j.biochi.2014.11.001

↑42. Weeks SD, Muranova LK, Heirbaut M, et al. Characterization of human small heat shock protein HSPB1 alpha-crystallin domain localized mutants associated with hereditary motor neuron diseases. Sci Rep. 2018;8(1):688. https://doi.org/10.1038/s41598-017-18874-x

↑43. Muranova LK, Weeks SD, Strelkov SV, Gusev NB. Characterization of Mutants of Human Small Heat Shock Protein HspB1 Carrying Replacements in the N-Terminal Domain and Associated with Hereditary Motor Neuron Diseases. PLoS One. 2015;10(5):e0126248. https://doi.org/10.1371/journal.pone.0126248

↑44. Samsonov MV, Khapchaev AY, Vorotnikov AV, et al. Impact of Atherosclerosis- and Diabetes-Related Dicarbonyls on Vascular Endothelial Permeability: A Comparative Assessment. Oxid Med Cell Longev. 2017;2017:1625130. https://doi.org/10.1155/2017/1625130

↑45. Maroni G, Tkachuk VA, Egorov A, et al. Prep1 prevents premature adipogenesis of mesenchymal progenitors. Sci Rep. 2017;7(1):15573. https://doi.org/10.1038/s41598-017-15828-1

↑46. Kulebyakin K, Penkov D, Blasi F, et al. The transcription factor Prep1 controls hepatic insulin sensitivity and gluconeogenesis by targeting nuclear localization of FOXO1. Biochem Biophys Res Commun. 2016;481(1-2):182-188. https://doi.org/10.1016/j.bbrc.2016.10.146

↑47. Ciccarelli M, Vastolo V, Albano L, et al. Glucose-induced expression of the homeotic transcription factor Prep1 is associated with histone post-translational modifications in skeletal muscle. Diabetologia. 2016;59(1):176-186. https://doi.org/10.1007/s00125-015-3774-6

↑48. Соркина Е.Л. Наследственные липодистрофии: клинические, гормональные и молекулярно-генетические характеристики: Автореф. дис.... канд. мед. наук. -М.; 2017. [Sorokina EL. Nasledstvennye lipodistrofii: klinicheskie, gormonal’nye i molekulyarno-geneticheskie kharakteristiki. [dissertation] Moscow; 2107.

↑49. Соркина Е.Л., Калашникова М.В., Мельниченко Г.А., Тюльпаков А.Н. Семейная парциальная липодистрофия (синдром Dunnigan) вследствие мутации в гене LMNA: первое описание клинического случая в России // Терапевтический архив. -2015. -№3. -С. 83-86. [Sorkina EL, Kalashnikova MV, Melnichenko GA, Tyulpakov AN. Familial partial lipodystrophy (Dunnigan syndrome) due to LMNA gene mutation: The first description of its clinical case in Russia. Ter Arkh. 2015;(3):83-86. (In Russ.)] https://doi.org/10.17116/terarkh201587383-87

↑50. Соркина Е.Л., Калашникова М.Ф., Лиходей Н.В., и др. Развитие метаболического синдрома в молодом возрасте как проявление семейной парциальной липодистрофии 3 типа (дефект гена PPARG): первое описание клинического случая в России // Сахарный диабет. -2015. -Т. 18. -№3. -С. 99-105. [Sorkina EL, Kalashnikova MF, Likhodey NV, et al. Development of metabolic syndrome at a young age as a manifestation of familial partial lipodystrophy type 3 (PPARG mutation): the first description of its clinical case in Russia. Diabetes mellitus.2015;18(3):99-105. (In Russ.)] https://doi.org/10.14341/DM2015399-105



↑51. Sorkina E, Frolova E, Rusinova D, et al. Progressive Generalized Lipodystrophy as a Manifestation of Autoimmune Polyglandular Syndrome Type 1. J Clin Endocrinol Metab. 2016;101(4):1344-1347. https://doi.org/10.1210/jc.2015-3722

↑52. Hussain I, Patni N, Ueda M, et al. A Novel Generalized Lipodystrophy-Associated Progeroid Syndrome Due to Recurrent Heterozygous LMNA p.T10I Mutation. J Clin Endocrinol Metab. 2018;103(3):1005-1014. https://doi.org/10.1210/jc.2017-02078

↑53. Brown RJ, Araujo-Vilar D, Cheung PT, et al. The Diagnosis and Management of Lipodystrophy Syndromes: A Multi-Society Practice Guideline. J Clin Endocrinol Metab. 2016;101(12):4500-4511. https://doi.org/10.1210/jc.2016-2466

↑54. Giorda CB, Sacerdote C, Nada E, et al. Incretin-based therapies and acute pancreatitis risk: a systematic review and meta-analysis of observational studies. Endocrine. 2015;48(2):461-471. https://doi.org/10.1007/s12020-014-0386-8

↑55. Mannucci E, Monami M. Cardiovascular Safety of Incretin-Based Therapies in Type 2 Diabetes: Systematic Review of Integrated Analyses and Randomized Controlled Trials. Adv Ther. 2017;34(1):1-40. https://doi.org/10.1007/s12325-016-0432-4

↑56. Xie W, Song X, Liu Z. Impact of dipeptidyl-peptidase 4 inhibitors on cardiovascular diseases. Vascul Pharmacol. 2018;109:17-26. https://doi.org/10.1016/j.vph.2018.05.010

↑57. Gomes GKA, de Camargos Ramos AI, de Sousa CT, et al. Linagliptin safety profile: A systematic review. Prim Care Diabetes. 2018. https://doi.org/10.1016/j.pcd.2018.04.006

Для цитирования:




Дедов И.И., Ткачук В.А., Гусев Н.Б., Ширинский В.П., Воротников А.В., Кочегура Т.Н., Майоров А.Ю., Шестакова М.В. Сахарный диабет 2 типа и метаболический синдром: молекулярные механизмы, ключевые сигнальные пути и определение биомишеней для новых лекарственных средств. Сахарныйдиабет. 2018;21(5):364-375.r citation:

Dedov I.I., Tkachuk V.A., Gusev N.B., Shirinsky V.P., Vorotnikov A.V., Kochegura T.N., Mayorov A.Yu., Shestakova M.V. Type 2 diabetes and metabolic syndrome: identification of the molecular mechanisms, key signaling pathways and transcription factors aimed to reveal new therapeutical targets. Diabetes mellitus. 2018;21(5):364-375. (In Russ.)

Просмотров: 1013


Контент доступен под лицензией Creative Commons Attribution 4.0 License.

ISSN 2072-0351 (Print)
ISSN 2072-0378 (Online)