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1Academic Journal
المؤلفون: V. V. Kalyuzhin, A. T. Teplyakov, I. D. Bespalova, E. V. Kalyuzhina, G. E. Chernogoryuk, N. N. Terentyeva, E. V. Grakova, K. V. Kopeva, V. Yu. Usov, N. P. Garganeeva, I. K. Livshits, I. V. Petrova, T. V. Lasukova, В. В. Калюжин, А. Т. Тепляков, И. Д. Беспалова, Е. В. Калюжина, Г. Э. Черногорюк, Н. Н. Терентьева, Е. В. Гракова, К. В. Копьева, В. Ю. Усов, Н. П. Гарганеева, И. К. Лившиц, И. В. Петрова, Т. В. Ласукова
المصدر: Bulletin of Siberian Medicine; Том 22, № 3 (2023); 98-109 ; Бюллетень сибирской медицины; Том 22, № 3 (2023); 98-109 ; 1819-3684 ; 1682-0363 ; 10.20538/1682-0363-2023-22-3
مصطلحات موضوعية: посттрансляционная модификация, diastolic heart failure, left ventricle, diastolic dysfunction, mechanisms, endosarcomeric cytoskeleton, titin, alternative splicing, post-translational modification, диастолическая сердечная недостаточность, левый желудочек, диастолическая дисфункция, механизмы, эндосаркомерный скелет, титин, альтернативный сплайсинг
وصف الملف: application/pdf
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Associations of ATP-sensitive potassium channel’s gene polymorphisms with type 2 diabetes and related cardiovascular phenotypes. Front. Cardiovasc. Med. 2022March23;9:816847. DOI:10.3389/fcvm.2022.816847.; https://bulletin.ssmu.ru/jour/article/view/5315
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2Academic Journal
المؤلفون: E. V. Grakova, K. V. Kopeva, S. N. Shilov, E. T. Bobyleva, E. N. Berezikova, V. V. Kalyuzhin, A. T. Teplyakov, Е. В. Гракова, К. В. Копьева, С. Н. Шилов, Е. Т. Бобылева, Е. Н. Березикова, В. В. Калюжин, А. Т. Тепляков
المساهمون: The study was carried out within the basic research “Study of the mechanisms of structural and functional myocardial remodeling in different phenotypes in heart failure of ischemic and non-ischemic etiology” No.122020300045-5, Фундаментальное научное исследование «Изучение механизмов структурного и функционального ремоделирования миокарда при разных фенотипах хронической сердечной недостаточности ишемической и неишемической этиологии» (№ 122020300045-5)
المصدر: Bulletin of Siberian Medicine; Том 22, № 3 (2023); 25-35 ; Бюллетень сибирской медицины; Том 22, № 3 (2023); 25-35 ; 1819-3684 ; 1682-0363 ; 10.20538/1682-0363-2023-22-3
مصطلحات موضوعية: прогноз, anthracyclines, humoral markers, prognosis, антрациклины, гуморальные маркеры
وصف الملف: application/pdf
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Heart Fail Rev. 2021;26(4):881–890. DOI:10.1007/s10741-020-10063-9.; Bansal N., Adams M.J., Ganatra S., Colan S.D., Aggarwal S., Steiner R. et al. Strategies to prevent anthracycline-induced cardiotoxicity in cancer survivors. Cardio-Oncology. 2019;5:1– 22. DOI:10.1186/s40959-019-0054-5.; Songbo M., Lang H., Xinyong C., Bin X., Ping Z., Liang S. Oxidative stress injury in doxorubicin-induced cardiotoxicity. Toxicol. Lett. 2019;307:41–48. DOI:10.1016/j.toxlet.2019.02.013.; Aminkeng F., Ross C.J., Rassekh S.R., Hwang S., Rieder M.J., Bhavsar A.P. et al. CPNDS Clinical Practice Recommendations Group. Recommendations for genetic testing to reduce the incidence of anthracycline-induced cardiotoxicity. Br. J. Clin. Pharmacol. 2016;82(3):683–695. DOI:10.1111/bcp.13008.; Lyon A.R., López-Fernández T., Couch L.S., Asteggiano R., Aznar M.C., Bergler-Klein J. et al. ESC Scientific Document Group. 2022 ESC Guidelines on cardio-oncology developed in collaboration with the European Hematology Association (EHA), the European Society for Therapeutic Radiology and Oncology (ESTRO) and the International Cardio-Oncology Society (IC-OS). Eur. Heart J. 20221;43(41):4229–4361. DOI:10.1093/eurheartj/ehac244.; Capranico G., Tinelli S., Austin C.A., Fisher M.L., Zunino F. Different patterns of gene expression of topoisomerase 2 isoforms in differentiated tissues during murine development. Biochim. Biophys. Acta. 1992;1132(1):43–48. DOI:10.1016/0167-4781(92)90050-A.; Grakova E.V., Shilov S.N., Kopeva K.V., Berezikova E.N., Popova A.A., Neupokoeva M.N. et al. Extracellular matrix remodeling in anthracycline-induced cardiotoxicity: What place on the pedestal? Int. J. Cardiol. 2022;350:55–61. DOI:10.1016/j.ijcard.2022.01.013.; Adamcová M., Potáčová A., Popelová O. et al. Cardiac remodeling and MMPs on the model of chronic daunorubicin-induced cardiomyopathy in rabbits. Physiol. Res. 2010;59(5):831–836. DOI:10.33549/physiolres.931797.; Saleh Y., Abdelkarim O., Herzallah K. Abela G.S. Anthracycline-induced cardiotoxicity: mechanisms of action, incidence, risk factors, prevention, and treatment. Heart Fail Rev. 2021;26(5):1159–1173. DOI:10.1007/s10741-020-09968-2.; Leerink J.M., van de Ruit M., Feijen E.A.M. et al. Extracellular matrix remodeling in animal models of anthracycline-induced cardiomyopathy: a meta-analysis. J. Mol. Med. (Berlin). 2021;99(9):1195–1207. DOI:10.1007/s00109-021-02098-8.; Octavia Y., Tocchetti C.G., Gabrielson K.L., Janssens S., Crijns H.J., Moens A.L. Doxorubicin-induced cardiomyopathy: from molecular mechanisms to therapeutic strategies. J. Mol. Cell Cardiol. 2012;52(6):1213–1225. DOI:10.1016/j.yjmcc.2012.03.006.; Vanhoutte D., Heymans S. TIMPs and cardiac remodeling: ‘embracing the MMP-independent-side of the family’. J. Mol. Cell Cardiol. 2010;48(3):445–453. DOI:10.1016/j.yjmcc.2009.09.013.; Schulz R. Intracellular targets of matrix metalloproteinase-2 in cardiac disease: rationale and therapeutic approaches. Annu. Rev. Pharmacol. Toxicol. 2007;47:211–242. DOI:10.1146/annurev.pharmtox.47.120505.105230.; Chan B.Y.H., Roczkowsky A., Cho W.J., Poirier M., Sergi C., Keschrumrus V. et al. MMP inhibitors attenuate doxorubicin cardiotoxicity by preventing intracellular and extracellular matrix remodeling. Cardiovasc. Res. 2021;117(1):188–200. DOI:10.1093/cvr/cvaa017.; Fanjul-Fernández M., Folgueras A.R., Cabrera S., LópezOtín C. Matrix metalloproteinases: Evolution, gene regulation and functional analysis in mouse models. Biochimica et Biophysica Acta (BBA) – Molecular Cell Research. 2010;1803(1):3–19. DOI:10.1016/j.bbamcr.2009.07.004.; Alfonso-Jaume M.A., Bergman M.R., Mahimkar R., Cheng S., Jin Z.Q., Karliner J.S. et al. 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DOI:10.1038/aps.2011.194.; Toro-Salazar O.H., Lee J.H., Zellars K.N., Perreault P.E., Mason K.C., Wang Z. et al. Use of integrated imaging and serum biomarker profiles to identify subclinical dysfunction in pediatric cancer patients treated with anthracyclines. Cardiooncology. 2018;4:4. DOI:10.1186/s40959-018-0030-5.; Wewer U.M., Ibaraki K., Schjørring P., Durkin M.E., Young M.F., Albrechtsen R. A potential role for tetranectin in mineralization during osteogenesis. J. Cell Biol. 1994;127(6Pt1):1767–1775. DOI:10.1083/jcb.127.6.1767.; Nielsen H., Clemmensen I., Kharazmi A. Tetranectin: a novel secretory protein from human monocytes. Scand. J. Immunol. 1993;37(1):39–42. DOI:10.1111/j.1365-3083.1993.tb01662.x.; Christensen L., Clemmensen I. Tetranectin immunoreactivity in normal human tissues. An immunohistochemical study of exocrine epithelia and mesenchyme. Histochemistry. 1989;92(1):29–35. DOI:10.1007/BF00495012.; Ho J.E., Lyass A., Courchesne P., Chen G., Liu C., Yin X. et al. 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Rep. 2015;5:17632. DOI:10.1038/srep17632.; Копьева К.В., Тепляков А.Т., Гракова Е.В., Солдатенко М.В., Огуркова О.Н., Ахмедов Ш.Д. Роль нового биомаркераST2 в оценке ремоделирования миокарда у больных хронической сердечной недостаточностью ишемического генеза с сохраненной фракцией выброса левого желудочка. Кардиология. 2018;58(10S):33–43. DOI:10.18087/cardio.2498.; Garbern J.C., Williams J., Kristl A.C., Malick A., Rachmin I., Gaeta B. et al. Dysregulation of IL-33/ST2 signaling and myocardial periarteriolar fibrosis. J. Mol. Cell Cardiol. 2019;128:179–186. DOI:10.1016/j.yjmcc.2019.01.018.; Останко В.Л., Калачева Т.П., Калюжина Е.В., Лившиц И.К., Шаловай А.А., Черногорюк Г.Э. и др. Биологические маркеры в стратификации риска развития и прогрессирования сердечно-сосудистой патологии: настоящее и будущее. Бюллетень сибирской медицины. 2018;17(4):264−280. DOI:10.20538/1682-0363-2018-4-264-280.; https://bulletin.ssmu.ru/jour/article/view/5302
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3Academic Journal
المؤلفون: K. V. Kopeva, A. N. Maltseva, E. V. Grakova, A. V. Mochula, M. V. Soldatenko, V. V. Kalyuzhin, K. V. Zavadovsky, К. В. Копьева, А. Н. Мальцева, Е. B. Гракова, А. В. Мочула, М. В. Солдатенко, В. В. Калюжин, К. В. Завадовский
المساهمون: The study was supported by the grant awarded by the President of the Russian Federation No. MK-4257.2022.3., Исследование выполнено при поддержке гранта Президента Российской Федерации № MK-4257.2022.3.
المصدر: Bulletin of Siberian Medicine; Том 22, № 1 (2023); 41-50 ; Бюллетень сибирской медицины; Том 22, № 1 (2023); 41-50 ; 1819-3684 ; 1682-0363 ; 10.20538/1682-0363-2023-22-1
مصطلحات موضوعية: натрийуретический пептид, preserved ejection fraction, myocardial flow reserve, prognosis, natriuretic peptide, сохраненная фракция выброса, резерв миокардиального кровотока, прогноз
وصف الملف: application/pdf
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DOI:10.1093/cvr/cvaa006.; Zhou W., Lee J.C.Y., Leung S.T., Lai A., Lee T.F., Chiang J.B. et al. , Long-term prognosis of patients with coronary microvascular disease using stress perfusion cardiac magnetic resonance. JACC Cardiovasc. Imaging. 2021;14(3):602–611. DOI:10.1016/j.jcmg.2020.09.034.; Liga R., Neglia D., Kusch A., Favilli B., Giorgetti A., Gimelli A. Prognostic role of dynamic CZT imaging in CAD patients: interaction between absolute flow and CAD burden. JACC Cardiovasc. Imaging. 2022;15(3):540–542. DOI:10.1016/j.jcmg.2021.09.030.; Boden W.E., O’Rourke R.A., Teo K.K., Hartigan P.M., Maron D.J., Kostuk W.J. et al. COURAGE Trial Research Group. Optimal medical therapy with or without PCI for stable coronary disease. N. Engl. J. Med. 2007;356(15):1503–1516. DOI:10.1056/NEJMoa070829.; Maron D.J., Hochman J.S., Reynolds H.R., Bangalore S., O’Brien S.M., Boden W.E. et al. ISCHEMIA Research Group. Initial invasive or conservative strategy for stable coronary disease. N. Engl. J. Med. 2020;382(15):1395–1407. DOI:10.1056/NEJMoa1915922.; Shimokawa H., Suda A., Takahashi J., Berry C., Camici P.G., Crea F. et al. Clinical characteristics and prognosis of patients with microvascular angina: an international and prospective cohort study by the Coronary Vasomotor Disorders International Study (COVADIS) Group. Eur. Heart J. 2021;42(44):4592–4600. DOI:10.1093/eurheartj/ehab282.; Schroder J., Michelsen M.M., Mygind N.D., Suhrs H.E., Bove K.B., Bechsgaard D.F. et al. Coronary flow velocity reserve predicts adverse prognosis in women with angina and no obstructive coronary artery disease: results from the iPOWER study. Eur. Heart J. 2021;42(3):228–239. DOI:10.1093/ eurheartj/ehaa944.; Kato S., Fukui K., Kodama S., Azuma M., Nakayama N., Iwasawa T. et al. Cardiovascular magnetic resonance assessment of coronary flow reserve improves risk stratification in heart failure with preserved ejection fraction. J. Cardiovasc. Magn. Reson. 2021;23(1):112. DOI:10.1186/s12968-02100807-3.; Lam J.H., Quah J.X., Davies T., Boos C.J., Nel K., Anstey C.M. et al. Relationship between coronary microvascular dysfunction and left ventricular diastolic function in patients with chest pain and unobstructed coronary arteries. Echocardiography. 2020;37(8):1199–1204. DOI:10.1111/echo.14794.; Snoer M., Monk-Hansen T., Olsen R.H., Pedersen L.R., Nielsen O.W., Rasmusen H. et al. Coronary flow reserve as a link between diastolic and systolic function and exercise capacity in heart failure. Eur. Heart J. Cardiovasc. Imaging. 2013;14(7):677–683. DOI:10.1093/ehjci/jes269.; Crea F., Bairey Merz C.N., Beltrame J.F., Kaski J.C., Ogawa H., Ong P., Sechtem U., Shimokawa H., Camici P.G. The parallel tales of microvascular angina and heart failure with preserved ejection fraction: a paradigm shift. Eur. Heart J. 2017;38(7):473–477. DOI:10.1093/eurheartj/ehw461.; Filali Y., Kesäniemi A., Ukkola O. Soluble ST2, a biomarker of fibrosis, is associated with multiple risk factors, chronic diseases and total mortality in the OPERA study. Scand. J. Clin. Lab. Invest. 2021;81(4):324–331. DOI:10.1080/00365513.2021.1904518.; https://bulletin.ssmu.ru/jour/article/view/5130
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4Academic Journal
المؤلفون: E. V. Grakova, K. V. Kopeva, S. N. Shilov, E. N. Berezikova, A. A. Popova, M. N. Neupokoeva, E. T. Ratushnyak, V. V. Kalyuzhin, A. T. Teplyakov, Е. В. Гракова, К. В. Копьева, С. Н. Шилов, Е. Н. Березикова, А. А. Попова, М. Н. Неупокоева, Е. Т. Ратушняк, В. В. Калюжин, А. Т. Тепляков
المساهمون: Basic research “Study of the mechanisms of structural and functional myocardial remodeling in different phenotypes in heart failure of ischemic and non-ischemic etiology” No. 122020300045-5, Фундаментальное научное исследование «Изучение механизмов структурного и функционального ремоделирования миокарда при разных фенотипах хронической сердечной недостаточности ишемической и неишемической этиологии» № 122020300045-5
المصدر: Bulletin of Siberian Medicine; Том 21, № 4 (2022); 44-53 ; Бюллетень сибирской медицины; Том 21, № 4 (2022); 44-53 ; 1819-3684 ; 1682-0363 ; 10.20538/1682-0363-2022-21-4
مصطلحات موضوعية: ингибитор ангиотензинпревращающего фермента, heart failure, gene polymorphisms, β-blocker, angiotensin-converting enzyme inhibitor, сердечная недостаточность, полиморфизмы генов, β-адреноблокатор
وصف الملف: application/pdf
Relation: https://bulletin.ssmu.ru/jour/article/view/5020/3301; https://bulletin.ssmu.ru/jour/article/view/5020/3326; Тепляков А.Т., Шилов С.Н., Попова А.А., Гракова Е.В., Березикова Е.Н., Неупокоева М.Н. и др. Состояние сердечно-сосудистой системы у больных с антрациклиновой кардиомиопатией. Бюллетень сибирской медицины. 2017;16(3):127–136. DOI:10.20538/1682-0363-2017-3-127136.; Kheiri B., Abdalla A., Osman M., Haykal T., Chahine A., Ahmed S. et al. Meta-Analysis of Carvedilol for the Prevention of Anthracycline-Induced Cardiotoxicity. Am. J. Cardiol. 2018;122(11):1959–1964. DOI:10.1016/j.amjcard.2018.08.039.; McCune C., McGowan M., Johnston R., McCarthy A., Watson C., Dixon L. The prevalence of late anthracycline induced cardiotoxicity in survivors of childhood malignancy in Northern Ireland. Heart. 2019;105:A52. DOI:10.1136/heartjnl-2019ICS.64.; Volkova M., Russell R. Anthracycline cardiotoxicity: prevalence, pathogenesis and treatment. Curr. Cardiol. Rev. 2011;7(4):214–220. DOI:10.2174/157340311799960645.; Janbabai G., Nabati M., Faghihinia M., Azizi S., Borhani S., Yazdani J. Effect of enalapril on preventing anthracycline-induced cardiomyopathy. Cardiovasc. Toxicol. 2017;17(2):130– 139. DOI:10.1007/s12012-016-9365-z.; Cardinale D., Colombo A., Lamantia G., Colombo N., Civelli M., De Giacomi G. et al. Anthracycline-induced cardiomyopathy: clinical relevance and response to pharmacologic therapy. J. Am. Coll. Cardiol. 2010;19;55(3):213–220. DOI:10.1016/j.jacc.2009.03.095.; Aminkeng F., Ross C.J., Rassekh S.R., Hwang S., Rieder M.J., Bhavsar A.P. et al. CPNDS Clinical Practice Recommendations Group. Recommendations for genetic testing to reduce the incidence of anthracycline-induced cardiotoxicity. Br. J. Clin. Pharmacol. 2016;82(3):683–695. DOI:10.1111/bcp.13008.; Elitok A., Oz F., Cizgici A.Y., Kilic L., Ciftci R., Sen F. et al. Effect of carvedilol on silent anthracycline-induced cardiotoxicity assessed by strain imaging: A prospective randomized controlled study with six-month follow-up. Cardiol. J. 2014;21(5):509–515. DOI:10.5603/CJ.a2013.0150.; Bansal N., Adams M.J., Ganatra S., Colan S.D., Aggarwal S., Steiner R. et al. Strategies to prevent anthracycline-induced cardiotoxicity in cancer survivors. Cardiooncology. 2019;2;5:18. DOI:10.1186/s40959-019-0054-5.; Book W.M. Carvedilol: a nonselective β blocking agent with antioxidant properties. Congestive Heart Failure. 2002;8:173– 190. DOI:10.1111/j.1527-5299.2002.00718.x.; Nabati M., Janbabai G., Baghyari S., Esmaili K., Yazdani J. Cardioprotective effects of carvedilol in inhibiting doxorubicin-induced cardiotoxicity. J. Cardiovasc. Pharmacol. 2017;69(5):279–285. DOI:10.1097/FJC.0000000000000470.; Avila M.S., Ayub-Ferreira S.M., de Barros Wanderley M.R. et al. Carvedilol for Prevention of ChemotherapyRelated Cardiotoxicity: The CECCY Trial. J. Am. Coll. Cardiol. 2018;22;71(20):2281–2290. DOI:10.1016/j.jacc.2018.02.049.; Guglin M., Krischer J., Tamura R., Fink A., Bello-Matricaria L., McCaskill-Stevens W. et al. Randomized Trial of Lisinopril Versus Carvedilol to Prevent Trastuzumab Cardiotoxicity in Patients With Breast Cancer. J. Am. Coll. Cardiol. 2019;11;73(22):2859–2868. DOI:10.1016/j.jacc.2019.03.495.; Cardinale D., Colombo A., Sandri M., Lamantia G., Colombo N., Civelli M. et al. Prevention of high-dose chemotherapy-induced cardiotoxicity in high-risk patients by angiotensin-converting enzyme inhibition. Circulation. 2006;5;114(23):2474–2481. DOI:10.1161/CIRCULATIONAHA.106.635144.; Silber J.H., Cnaan A., Clark B.J., Paridon S.M., Chin A.J., Rychik J. et al. Enalapril to prevent cardiac function decline in long-term survivors of pediatric cancer exposed to anthracyclines. J. Clin. Oncol. 2004;1;22(5):820–828. DOI:10.1200/JCO.2004.06.022.; Bosch X., Rovira M., Sitges M., Domènech A., Ortiz-Pérez J.T., de Caralt T.M. et al. Enalapril and carvedilol for preventing chemotherapy-induced left ventricular systolic dysfunction in patients with malignant hemopathies: the OVERCOME trial (preventiOn of left Ventricular dysfunction with Enalapril and caRvedilol in patients submitted to intensive ChemOtherapy for the treatment of Malignant hEmopathies). J. Am. Coll. Cardiol. 2013;11;61(23):2355–2362. DOI:10.1016/j.jacc.2013.02.072.; Nazarenko M.S., Markov A.V., Sleptsov A.A. et al. Comparative analysis of gene expression in vascular cells of patients with advanced atherosclerosis. Biomed. Khim. 2018;64(5):416–442. DOI:10.18097/PBMC20186405416.; Brodde O.E. Beta1and beta2-adrenoceptor polymorphisms and cardiovascular diseases. Fundam. Clin. Pharmacol. 2008;22(2):107–125. DOI:10.1111/j.1472-8206.2007.00557.x.; Baudhuin L.M., Miller W.L., Train L., Bryant S., Hartman K.A., Phelps M. et al. Relation of ADRB1, CYP2D6, and UGT1A1 polymorphisms with dose of, and response to, carvedilol or metoprolol therapy in patients with chronic heart failure. Am. J. Cardiol. 2010;1;106(3):402–408. DOI:10.1016/j.amjcard.2010.03.041.; Metra M., Covolo L., Pezzali N., Zacà V., Bugatti S., Lombardi C. et al. Role of beta-adrenergic receptor gene polymorphisms in the long-term effects of beta-blockade with carvedilol in patients with chronic heart failure. Cardiovasc. Drugs Ther. 2010;24(1):49–60. DOI:10.1007/s10557-010-6220-5.; Chen L., Meyers D., Javorsky G., Burstow D. et al. Arg389Gly-beta1-adrenergic receptors determine improvement in left ventricular systolic function in nonischemic cardiomyopathy patients with heart failure after chronic treatment with carvedilol. Pharmacogenet. Genomics. 2007;17(11):941–949. DOI:10.1097/FPC.0b013e3282ef7354.; Luzum J.A., Sweet K.M., Binkley P.F., Schmidlen T.J., Jarvis J.P., Christman M.F. et al. CYP2D6 genetic variation and beta-blocker maintenance dose in patients with heart failure. Pharm. Res. 2017;34(8):1615–1625. DOI:10.1007/s11095017-2104-8.; Shihmanter R., Nulman I., Goland S., Caspi A., Bar-Haim A., Harary I. et al. Variation in the CYP2D6 genotype is not associated with carvedilol dose changes in patients with heart failure. J. Clin. Pharm. Ther. 2014;39(4):432–438. DOI:10.1111/jcpt.12154.; Katsarou M.S., Karathanasopoulou A., Andrianopoulou A., Desiniotis V., Tzinis E., Dimitrakis E. et al. Beta 1, Beta 2 and Beta 3 adrenergic receptor gene polymorphisms in a southeastern European population. Front. Genet. 2018;28;9:560. DOI:10.3389/fgene.2018.00560.; Uemura K., Nakura J., Kohara K. Miki T. Association of ACE I/D polymorphism with cardiovascular risk factors. Hum Genet. 2000; 107(3):239-42. doi:10.1007/s004390000358.; Niu T., Chen X., Xu X. Angiotensin converting enzyme gene insertion/deletion polymorphism and cardiovascular disease: therapeutic implications. Drugs. 2002;62(7):977–993. DOI:10.2165/00003495-200262070-00001.; https://bulletin.ssmu.ru/jour/article/view/5020
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5Academic Journal
المؤلفون: I. D. Bespalova, V. V. Kalyuzhin, B. Yu. Murashev, I. A. Osikhov, Yu. I. Koshchavtseva, A. V. Teteneva, D. S. Romanov, U. M. Strashkova, И. Д. Беспалова, В. В. Калюжин, Б. Ю. Мурашев, И. А. Осихов, Ю. И. Кощавцева, А. В. Тетенева, Д. С. Романов, У. М. Страшкова
المصدر: The Siberian Journal of Clinical and Experimental Medicine; Том 37, № 3 (2022); 114-120 ; Сибирский журнал клинической и экспериментальной медицины; Том 37, № 3 (2022); 114-120 ; 2713-265X ; 2713-2927
مصطلحات موضوعية: активные формы кислорода, visceral adipose tissue, adipose tissue inflammation, subpopulation composition of cells, reactive oxygen species, висцеральная жировая ткань, воспаление жировой ткани, субпопуляционный состав клеток
وصف الملف: application/pdf
Relation: https://cardiotomsk.elpub.ru/jour/article/view/1512/735; Ким О.Т., Драпкина О.М. Эпидемия ожирения через призму эволюционных процессов. Кардиоваскулярная терапия и профилактика. 2022;21(1):3109. DOI:10.15829/1728-8800-2022-3109.; Manna P., Jain S.K. Obesity, oxidative stress, adipose tissue dysfunction, and the associated health risks: Causes and therapeutic strategies. Metab. Syndr. Relat. Disord. 2015;13(10):423–444. DOI:10.1089/met.2015.0095.; Беспалова И.Д., Бычков В.А., Калюжин В.В., Рязанцева Н.В., Медянцев Ю.А., Осихов И.А. и др. Качество жизни больных гипертонической болезнью с метаболическим синдромом: взаимосвязь с маркерами системного воспаления. Бюллетень сибирской медицины. 2013;12(6):5–11. DOI:10.20538/1682-0363-2013-6-5-11.; Jankowska A., Brzeziński M., Romanowicz-Sołtyszewska A., Szlagatys Sidorkiewicz A. Metabolic syndrome in obese children-clinical prevalence and risk factors. Int. J. Environ. Res. Public Health. 2021;18(3):1060. DOI:10.3390/ijerph18031060.; Fernández-Sánchez A., Madrigal-Santillán E., Bautista M., Esquivel-Soto J., Morales-González A., Esquivel-Chirino C. et al. Infl ammation, oxidative stress, and obesity. Int. J. Mol. Sci. 2011;12(5):3117–3132. DOI:10.3390/ijms12053117.; Engin A. The pathogenesis of obesity-associated adipose tissue infl ammation. Adv. Exp. Med. Biol. 2017;960:221–245. DOI:10.1007/978-3-319-48382-5_9.; Flores-Cortez Y.A., Barragán-Bonilla M.I., Mendoza-Bello J.M., González-Calixto C., Flores-Alfaro E., Espinoza-Rojo M. Interplay of retinol binding protein 4 with obesity and associated chronic alterations (Review). Mol. Med. Res. 2022;26(1). DOI:10.3892/mmr.2022.12760.; Liu W., Zhou H., Wang H., Zhang Q., Zhang R., Willard B. et al. IL-1R-IRAKM-Slc25a1 signaling axis reprograms lipogenesis in adipocytes to promote diet-induced obesity in mice. Nat. Commun. 2022;13(1):2748. DOI:10.1038/s41467-022-30470-w.; Wang L., Gao T., Li Y., Xie Y., Zeng S., Tai C. et al. A long-term anti-infammation markedly alleviated high-fat diet-induced obesity by repeated administrations of overexpressing IL10 human umbilical cord-derived mesenchymal stromal cells. Stem Cell Res. Ther. 2022;13(1):259. DOI:10.1186/s13287-022-02935-8.; Hachiya R., Tanaka M., Itoh M., Suganami T. Molecular mechanism of crosstalk between immune and metabolic systems in metabolic syndrome. Infl amm. Regen. 2022;42(1):13. DOI:10.1186/s41232-022-00198-7.; Kawai T., Autieri M.V., Scalia R. Adipose tissue infl ammation and metabolic dysfunction in obesity. Am. J. Physiol. Cell Physiol. 2021;320(3):C375–C391. DOI:10.1152/ajpcell.00379.2020.; Криволапов Ю.А., Леенман Е.Е. Морфологическая диагностика лимфом. СПб: КОСТА; 2006:208.; Беспалова И.Д., Рязанцева Н.В., Калюжин В.В., Дзюман А.Н., Осихов И.А., Медянцев Ю.А. и др. Клинико-морфологические параллели при абдоминальном ожирении. Бюллетень Сибирского отделения Российской академии медицинских наук. 2014;34(4):51–58.; Zhang X., Liu Z., Li W., Kang Y., Xu Z., Li X. et al. MAPKs/AP-1, not NF-κB, is responsible for MCP-1 production in TNF-α-activated adipocytes. Adipocyte. 2022;11(1):477–486. DOI:10.1080/21623945.2022.2107786.; Nour O.A., Ghoniem H.A., Nader M.A., Suddek Gh.M. Impact of protocatechuic acid on high fat diet-induced metabolic syndrome sequelae in rats. European Journal of Pharmacology. 2021;907:174257. DOI:10.1016/j.ejphar.2021.174257.; Кологривова И.В., Суслова Т.Е., Кошельская О.А., Ребенкова М.С., Харитонова О.А., Андреев С.Л. и др. Макрофаги в эпикардиальной жировой ткани и сывороточный NT-proBNP у пациентов со стабильной ишемической болезнью сердца. Медицинская иммунология. 2022;24(2):389–394. DOI:10.15789/0000-0003-4049-8715.; Часовских Н.Ю., Рязанцева Н.В., Новицкий В.В. Апоптоз и окислительный стресс. Томск: Печатная мануфактура; 2009:148.; Иванов В.В., Шахристова Е.В., Степовая Е.А., Носарева О.Л., Фёдорова Т.С., Рязанцева Н.В. и др. Окислительный стресс: влияние на секрецию инсулина, рецепцию гормона адипоцитами и липолиз в жировой ткани. Бюллетень сибирской медицины. 2014;13(3):32–39. DOI:10.20538/1682-0363-2014-3-32-39.; Hotamisligil G.S. Endoplasmic reticulum stress and the infl ammatory basis of metabolic disease. Cell. 2010;140(6):900–917. DOI:10.1016/j.cell.2010.02.034.; https://cardiotomsk.elpub.ru/jour/article/view/1512
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6Academic Journal
المؤلفون: V. V. Kalyuzhin, A. T. Teplyakov, I. D. Bespalova, E. V. Kalyuzhina, N. N. Terentyeva, E. V. Grakova, K. V. Kopeva, V. Yu. Usov, N. P. Garganeeva, O. A. Pavlenko, Yu. V. Gorelova, A. V. Teteneva, В. В. Калюжин, А. Т. Тепляков, И. Д. Беспалова, Е. В. Калюжина, Н. Н. Терентьева, Е. В. Гракова, К. В. Копьева, В. Ю. Усов, Н. П. Гарганеева, О. А. Павленко, Ю. В. Горелова, А. В. Тетенева
المصدر: Bulletin of Siberian Medicine; Том 21, № 3 (2022); 181-197 ; Бюллетень сибирской медицины; Том 21, № 3 (2022); 181-197 ; 1819-3684 ; 1682-0363 ; 10.20538/1682-0363-2022-21-3
مصطلحات موضوعية: имплантация аппарата вспомогательного кровообращения, treatment, neurohormonal modulators, sacubitril / valsartan, pecavaptan, fineron, vericiguat, sodium – glucose cotransporter type 2 inhibitors, omecamtiv mecarbil, gene therapy, cardiac resynchronization therapy, cardiac contractility modulation, heart transplantation, implantation of a circulatory assist device, лечение, нейрогормональные модуляторы, сакубитрил/валсартан, пекаваптан, финерон, верицигуат, ингибиторы натрий-глюкозного котранспортера 2-го типа, омекамтив мекарбил, генная терапия, сердечная ресинхронизирующая терапия, модуляция сердечной сократимости, трансплантация сердца
وصف الملف: application/pdf
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7Academic Journal
المؤلفون: V. V. Kalyuzhin, A. T. Teplyakov, I. D. Bespalova, E. V. Kalyuzhina, N. N. Terentyeva, I. K. Livshits, V. L. Ostanko, E. V. Grakova, K. V. Kopeva, V. Yu. Usov, N. P. Garganeeva, Yu. V. Gorelova, В. В. Калюжин, А. Т. Тепляков, И. Д. Беспалова, Е. В. Калюжина, Н. Н. Терентьева, И. К. Лившиц, В. Л. Останко, Е. В. Гракова, К. В. Копьева, В. Ю. Усов, Н. П. Гарганеева, Ю. В. Горелова
المصدر: Bulletin of Siberian Medicine; Том 21, № 2 (2022); 152-167 ; Бюллетень сибирской медицины; Том 21, № 2 (2022); 152-167 ; 1819-3684 ; 1682-0363 ; 10.20538/1682-0363-2022-21-2
مصطلحات موضوعية: ультрафильтрация, diuretic resistance, terminology, mechanisms, water and salt restriction, sequential nephron blockade, gliflozines, vaptans, inotropes, vasoconstrictors, glucocorticoids, serelaxin, nesiritide, albumin, ultrafiltration, резистентность к диуретикам, терминология, механизмы, водно-солевой режим, секвенциальная блокада нефрона, глифлозины, ваптаны, инотропы, вазоконстрикторы, глюкокортикостероиды, серелаксин, несиритид, альбумин
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