CardioSomaticsCardioSomaticsCardioСоматика2221-71852658-5707Eco-Vector62547310.17816/CS625473ReviewsОбзорыReview ArticleKlotho protein, fibroblast growth factor 23, and sclerostin in chronic heart failure: literature reviewБелок Klotho, фактор роста фибробластов 23 и склеростин при хронической сердечной недостаточности: обзор литературыhttps://orcid.org/0000-0001-5416-8579AlievaAmina M.АлиеваАмина Магомедовна
Russian Federation

MD, Cand. Sci. (Med.), associate professor

канд. мед. наук, доцент

amisha_alieva@mail.ruhttps://orcid.org/0000-0001-7479-418XReznikElena V.РезникЕлена Владимировна
Russian Federation

MD, Dr. Sci. (Med.), department head

д-р мед. наук, заведующая кафедрой

elenaresnik@gmail.comhttps://orcid.org/0000-0001-5352-8499KotikovaIrina A.КотиковаИрина Александровна
Russian Federation

student

студентка

kotikova.ia@mail.ruhttps://orcid.org/0000-0003-1699-0881NikitinIgor G.НикитинИгорь Геннадиевич
Russian Federation

MD, Dr. Sci. (Med.), Professor

д-р мед. наук, профессор

igor.nikitin.64@mail.ruPirogov Russian National Research Medical UniversityРоссийский национальный исследовательский медицинский университет им. Н.И. Пирогова280320241004202415141530501202431012024Copyright ©; 2024, Eco-VectorCopyright ©; 2024, ООО "Эко-Вектор"2024Eco-VectorООО "Эко-Вектор"https://creativecommons.org/licenses/by-nc-nd/4.0/https://cardiosomatics.ru/2221-7185/article/view/625473

Chronic heart failure (CHF) is a global medical, social, and economic problem. It is a syndrome caused by imbalanced neurohumoral regulation of the cardiovascular system, which is accompanied by impaired systolic and/or diastolic function of the heart. Currently, the search and study of new biological markers that can help in the early diagnosis of CHF, serve as a laboratory tool for assessing treatment effectiveness, or be used as prognostic markers and risk stratification criteria are ongoing. Researchers focused on studying the role of Klotho protein, fibroblast growth factor 23 (FGF23), and sclerostin in patients with CHF. Klotho expression decreases as the body ages, and impaired production has been reported in various aging-related diseases. The FGF23 / Klotho axis plays a key regulatory role in cardiovascular pathology. Laboratory, clinical, and genetic studies have suggested that sclerostin is associated with heart disease, although available data are not entirely consistent. Clinical work conducted on the study of the Klotho protein, FGF-23, and sclerostin indicates the potentially important diagnostic and prognostic significance of their analysis in patients with CHF. Thus, more studies of the issues related to serial testing of these biological markers, including in the aspect of the multibiomarker model, are needed.

Хроническая сердечная недостаточность (ХСН) является глобальной медицинской, социальной и экономической проблемой. ХСН — это синдром, обусловленный дисбалансом нейрогуморальной регуляции сердечно-сосудистой системы, который сопровождается нарушением систолической и/или диастолической функции сердца. В настоящее время продолжаются поиск и изучение новых биологических маркёров, способных обеспечить раннюю диагностику ХСН, служить лабораторным инструментом для оценки эффективности проводящегося лечения или использоваться в качестве прогностических маркёров и критериев стратификации риска. Интерес исследователей сосредоточен на изучении роли белка Klotho, фактора роста фибробластов 23 (FGF23) и склеростина у пациентов с ХСН. Интенсивность экспрессии Klotho уменьшается по мере старения организма, дефекты его выработки были зарегистрированы при различных заболеваниях, ассоциированных со старением. Ось FGF23 / Klotho играет ключевую регуляторную роль при кардиоваскулярной патологии. Триангуляция данных лабораторных, клинических и генетических исследований позволяет предположить, что склеростин связан с заболеваниями сердца, хотя полученные к настоящему времени данные не вполне согласуются друг с другом. Проведённые клинические исследования, посвящённые изучению белка Klotho, FGF-23 и склеростина, указывают на потенциально важную диагностическую и прогностическую значимость их анализа у пациентов с ХСН. Вопросы, связанные с серийным тестированием этих биологических маркёров, в том числе и в аспекте мультибиомаркёрной модели, нуждаются в дальнейшем изучении.

biological markerscardiovascular diseasesKlotho proteinfibroblast growth factor 23sclerostinбиологические маркёрысердечно-сосудистые заболеваниябелок Klothoфактор роста фибробластов 23склеростинRiccardi M, Sammartino AM, Piepoli M, et al. Heart failure: an update from the last years and a look at the near future. ESC Heart Fail. 2022;9(6):3667–3693. doi: 10.1002/ehf2.14257. Erratum in: ESC Heart Fail. 2023;10(3):2143.Riccardi M., Sammartino A., Piepoli M., et al. Heart failure: an update from the last years and a look at the near future // ESC Heart Fail. 2022. Vol. 9, N 6. P. 3667–3693. doi: 10.1002/ehf2.14257. Erratum in: ESC Heart Fail. 2023. Vol. 10, N 3. P. 2143.Golukhova EZ, Alieva AM. Clinical value of natriuretic peptides detection at the patients with chronic heart failure. Kardiologiya i Serdechno-Sosudistaya Khirurgiya. 2007;(1):45–51. EDN: HGTYXSГолухова Е.З., Алиева А.М. Клиническое значение определения натрийуретических пептидов у больных с хронической сердечной недостаточностью // Кардиология и сердечно- сосудистая хирургия. 2007. № 1. С. 45–51. EDN: HGTYXSBozkurt B, Coats AJ, Tsutsui H, et al. Universal Definition and Classification of Heart Failure: A Report of the Heart Failure Society of America, Heart Failure Association of the European Society of Cardiology, Japanese Heart Failure Society and Writing Committee of the Universal Definition of Heart Failure. J Card Fail. 2021:S1071-9164(21)00050-6. doi: 10.1016/j.cardfail.2021.01.022. Epub ahead of print.Bozkurt B., Coats A., Tsutsui H., et al. Universal Definition and Classification of Heart Failure: A Report of the Heart Failure Society of America, Heart Failure Association of the European Society of Cardiology, Japanese Heart Failure Society and Writing Committee of the Universal Definition of Heart Failure// J Card Fail. 2021. S1071-9164(21)00050-6. doi: 10.1016/j.cardfail.2021.01.022. Epub ahead of print.Szlagor M, Dybiec J, Młynarska E, et al. Chronic Kidney Disease as a Comorbidity in Heart Failure. Int J Mol Sci. 2023;24(3):2988. doi: 10.3390/ijms24032988Szlagor M., Dybiec J., Młynarska E., et al. Chronic Kidney Disease as a Comorbidity in Heart Failure // Int J Mol Sci. 2023. Vol. 24, N 3. P. 2988. doi: 10.3390/ijms24032988Golukhova EZ, Teryaeva NB, Alieva AM. Natriuretic peptides — markers and prognosis factors in chronic heart failure. Creative Cardiology. 2007;(1–2):126–136. (In Russ.) EDN: KAOPTVГолухова Е.З., Теряева Н.Б., Алиева А.М. Натрийуретические пептиды — маркеры и факторы прогноза при хронической сердечной недостаточности // Креативная кардиология. 2007. № 1–2. C. 126–136. EDN: KAOPTVKuro-o M, Matsumura Y, Aizawa H, et al. Mutation of the mouse klotho gene leads to a syndrome resembling ageing. Nature. 1997;390(6655):45–51. doi: 10.1038/36285Kuro-o M., Matsumura Y., Aizawa H., et al. Mutation of the mouse klotho gene leads to a syndrome resembling ageing // Nature. 1997. Vol. 390, N 6655. P. 45–51. doi: 10.1038/36285Alieva AM, Reznik EV, Teplova NV, et al. Klotho protein and atherosclerotic cardiovascular diseases: prolonging the thread of life. Russian Medicine. 2022;28(5):365–380. doi: 10.17816/medjrf110823Алиева А.М., Резник Е.В., Теплова Н.В., и др. Белок Klotho и атеросклеротические сердечно-сосудистые заболевания: продлевая нить жизни // Российский медицинский журнал. 2022. Т. 28, № 5. С. 365–380. doi: 10.17816/medjrf110823Liu Y, Chen M. Emerging role of α-Klotho in energy metabolism and cardiometabolic diseases. Diabetes Metab Syndr. 2023;17(10):102854. doi: 10.1016/j.dsx.2023.102854Liu Y., Chen M. Emerging role of α-Klotho in energy metabolism and cardiometabolic diseases // Diabetes Metab Syndr. 2023. Vol. 17, N 10. P. 102854. doi: 10.1016/j.dsx.2023.102854Prud'homme GJ, Kurt M, Wang Q. Pathobiology of the Klotho Antiaging Protein and Therapeutic Considerations. Front Aging. 2022;(3):931331. doi: 10.3389/fragi.2022.931331Prud'homme G., Kurt M., Wang Q. Pathobiology of the Klotho Antiaging Protein and Therapeutic Considerations // Front Aging. 2022. N 3. P. 931331. doi: 10.3389/fragi.2022.931331Tobias JH. Sclerostin and Cardiovascular Disease. Curr Osteoporos Rep. 2023;21(5):519–526. doi: 10.1007/s11914-023-00810-wTobias J. Sclerostin and Cardiovascular Disease // Curr Osteoporos Rep. 2023. Vol. 21, N 5. P. 519–526. doi: 10.1007/s11914-023-00810-wOlejnik A, Franczak A, Krzywonos-Zawadzka A, et al. The Biological Role of Klotho Protein in the Development of Cardiovascular Diseases. Biomed Res Int. 2018;(2018):5171945. doi: 10.1155/2018/5171945. Erratum in: Biomed Res Int. 2020;(2020):1463925.Olejnik A., Franczak A., Krzywonos-Zawadzka A., et al. The Biological Role of Klotho Protein in the Development of Cardiovascular Diseases // Biomed Res Int. 2018. N 2018. P. 5171945. doi: 10.1155/2018/5171945. Erratum in: Biomed Res Int. 2020. N 2020. P. 1463925.Alieva AM, Pinchuk TV, Kislyakov VA, et al. Fibroblast growth factor-23 (fgf23) is a novel biological marker in heart failure. KMJ. 2022;(1):59–65. doi: 10.26269/pygh-k050Алиева А.М., Пинчук Т.В., Кисляков В.А., и др. Фактор роста фибробластов (FGF23) — новый биологический маркер при сердечной недостаточности // Кремлевская медицина. Клинический вестник. 2022. № 1. С. 59–65. doi: 10.26269/pygh-k050Kuro-O M. The Klotho proteins in health and disease. Nat Rev Nephrol. 2019;15(1):27–44. doi: 10.1038/s41581-018-0078-3Kuro-O M. The Klotho proteins in health and disease // Nat Rev Nephrol. 2019. Vol. 15, N 1. P. 27–44. doi: 10.1038/s41581-018-0078-3Thomas SM, Li Q, Faul C. Fibroblast growth factor 23, klotho and heparin. Curr Opin Nephrol Hypertens. 2023;32(4):313–323. doi: 10.1097/MNH.0000000000000895Thomas S., Li Q., Faul C. Fibroblast growth factor 23, klotho and heparin // Curr Opin Nephrol Hypertens. 2023. Vol. 32, N 4. P. 313–323. doi: 10.1097/MNH.0000000000000895Chen G, Liu Y, Goetz R, et al. α-Klotho is a non-enzymatic molecular scaffold for FGF23 hormone signalling. Nature. 2018;553(7689):461–466. doi: 10.1038/nature25451Chen G., Liu Y., Goetz R., et al. α-Klotho is a non-enzymatic molecular scaffold for FGF23 hormone signaling // Nature. 2018. Vol. 553, N 7689. P. 461–466. doi: 10.1038/nature25451Ranjbar N, Raeisi M, Barzegar M, et al. The possible anti-seizure properties of Klotho. Brain Res. 2023;(1820):148555. doi: 10.1016/j.brainres.2023.148555Ranjbar N., Raeisi M., Barzegar M., et al. The possible anti-seizure properties of Klotho // Brain Res. 2023. N 1820. P. 148555. doi: 10.1016/j.brainres.2023.148555Masuda H, Chikuda H, Suga T, et al. Regulation of multiple ageing-like phenotypes by inducible klotho gene expression in klotho mutant mice. Mech Ageing Dev. 2005;126(12):1274–1283. doi: 10.1016/j.mad.2005.07.007Masuda H., Chikuda H., Suga T., et al. Regulation of multiple ageing-like phenotypes by inducible klotho gene expression in klotho mutant mice // Mech Ageing Dev. 2005. Vol. 126, N 12. P. 1274–1283. doi: 10.1016/j.mad.2005.07.007Espuch-Oliver A, Vázquez-Lorente H, Jurado-Fasoli L, et al. References Values of Soluble α-Klotho Serum Levels Using an Enzyme-Linked Immunosorbent Assay in Healthy Adults Aged 18–85 Years. J Clin Med. 2022;11(9):2415. doi: 10.3390/jcm11092415Espuch-Oliver A., Vazquez-Lorente H., Jurado-Fasoli L., et al. References Values of Soluble α-Klotho Serum Levels Using an Enzyme-Linked Immunosorbent Assay in Healthy Adults Aged 18–85 Years // J Clin Med. 2022. Vol. 11, N 9. P. 2415. doi: 10.3390/jcm11092415Kresovich JK, Bulka CM. Low Serum Klotho Associated With All-cause Mortality Among a Nationally Representative Sample of American Adults. J Gerontol A Biol Sci Med Sci. 2022;77(3):452–456. doi: 10.1093/gerona/glab308Kresovich J., Bulka C. Low serum klotho associated with all-cause mortality among a nationally representative sample of American adults // J Gerontol A Biol Sci Med Sci. 2022. Vol. 3, N 3. P. 452–456. doi: 10.1093/gerona/glab308Li L, Liu W, Mao Q, et al. Klotho Ameliorates Vascular Calcification via Promoting Autophagy. Oxid Med Cell Longev. 2022;(2022):7192507. doi: 10.1155/2022/7192507Li L., Liu W., Mao Q., et al. Klotho Ameliorates Vascular Calcification via Promoting Autophagy // Oxid Med Cell Longev. 2022. N 2022. P. 7192507. doi: 10.1155/2022/7192507Mencke R, Hillebrands JL; NIGRAM consortium. The role of the anti-ageing protein Klotho in vascular physiology and pathophysiology. Ageing Res Rev. 2017;(35):124–146. doi: 10.1016/j.arr.2016.09.001Mencke R., Hillebrands J; NIGRAM consortium. The role of the anti-ageing protein Klotho in vascular physiology and pathophysiology// Ageing Res Rev. 2017. N 35. P. 124–146. doi: 10.1016/j.arr.2016.09.001Wang Y, Wang K, Bao Y, et al. The serum soluble Klotho alleviates cardiac aging and regulates M2a/M2c macrophage polarization via inhibiting TLR4/Myd88/NF-κB pathway. Tissue Cell. 2022;(76):101812. doi: 10.1016/j.tice.2022.101812Wang Y., Wang K., Bao Y., et al. The serum soluble Klotho alleviates cardiac aging and regulates M2a/M2c macrophage polarization via inhibiting TLR4/Myd88/NF-κB pathway // Tissue Cell. 2022. N 76. P. 101812. doi: 10.1016/j.tice.2022.101812Li X, Zhai Y, Yao Q, et al. Up-regulation of Myocardial Klotho Expression to Promote Cardiac Functional Recovery in Old Mice following Endotoxemia. Res Sq [Preprint]. 2023:rs.3.rs-2949854. doi: 10.21203/rs.3.rs-2949854/v1Li X., Zhai Y., Yao Q., et al. Up-regulation of Myocardial Klotho Expression to Promote Cardiac Functional Recovery in Old Mice following Endotoxemia // Res Sq [Preprint]. 2023. rs.3.rs-2949854. doi: 10.21203/rs.3.rs-2949854/v1Ding J, Tang Q, Luo B, et al. Klotho inhibits angiotensin II-induced cardiac hypertrophy, fibrosis, and dysfunction in mice through suppression of transforming growth factor-β1 signaling pathway. Eur J Pharmacol. 2019;(859):172549. doi: 10.1016/j.ejphar.2019.172549Ding J., Tang Q., Luo B., et al. Klotho inhibits angiotensin II-induced cardiac hypertrophy, fibrosis, and dysfunction in mice through suppression of transforming growth factor-β1 signaling pathway// Eur J Pharmacol. 2019. N 859. P. 172549. doi: 10.1016/j.ejphar.2019.172549Wang K, Li Z, Li Y, et al. Cardioprotection of Klotho against myocardial infarction-induced heart failure through inducing autophagy. Mech Ageing Dev. 2022;(207):111714. doi: 10.1016/j.mad.2022.111714Wang K., Li Z., Li Y., et al. Cardioprotection of Klotho against myocardial infarction-induced heart failure through inducing autophagy// Mech Ageing Dev. 2022. N 207. P. 111714. doi: 10.1016/j.mad.2022.111714Kamel SS, Baky NAA, Karkeet RM, et al. Astaxanthin extenuates the inhibition of aldehyde dehydrogenase and Klotho protein expression in cyclophosphamide-induced acute cardiomyopathic rat model. Clin Exp Pharmacol Physiol. 2022;49(2):291–301. doi: 10.1111/1440-1681.13598Kamel S., Baky N., Karkeet R., et al. Astaxanthin extenuates the inhibition of aldehyde dehydrogenase and Klotho protein expression in cyclophosphamide-induced acute cardiomyopathic rat model // Clin Exp Pharmacol Physiol. 2022. Vol. 49, N 2. P. 291–301. doi: 10.1111/1440-1681.13598Zhuang X, Sun X, Zhou H, et al. Klotho attenuated Doxorubicin-induced cardiomyopathy by alleviating Dynamin-related protein 1-mediated mitochondrial dysfunction. Mech Ageing Dev. 2021;(195):111442. doi: 10.1016/j.mad.2021.111442Zhuang X., Sun X., Zhou H., et al. Klotho attenuated Doxorubicin-induced cardiomyopathy by alleviating Dynamin-related protein 1-mediated mitochondrial dysfunction // Mech Ageing Dev. 2021. N 195. P. 111442. doi: 10.1016/j.mad.2021.111442Chen WY. Soluble Alpha-Klotho Alleviates Cardiac Fibrosis without Altering Cardiomyocytes Renewal. Int J Mol Sci. 2020;21(6):2186. doi: 10.3390/ijms21062186Chen W. Soluble Alpha-Klotho Alleviates Cardiac Fibrosis without Altering Cardiomyocytes Renewal // Int J Mol Sci. 2020. Vol. 21, N 6. P. 2186. doi: 10.3390/ijms21062186Xiong X, Wang G, Wang Y, et al. Klotho protects against aged myocardial cells by attenuating ferroptosis. Exp Gerontol. 2023;(175):112157. doi: 10.1016/j.exger.2023.112157Xiong X., Wang G., Wang Y., et al. Klotho protects against aged myocardial cells by attenuating ferroptosis // Exp Gerontol. 2023. N 175. P. 112157. doi: 10.1016/j.exger.2023.112157Cai J, Zhang L, Chen C, et al. Association between serum Klotho concentration and heart failure in adults, a cross-sectional study from NHANES 2007-2016. Int J Cardiol. 2023;(370):236–243. doi: 10.1016/j.ijcard.2022.11.010Cai J., Zhang L., Chen C., et al. Association between serum Klotho concentration and heart failure in adults, a cross-sectional study from NHANES 2007-2016 // Int J Cardiol. 2023. N 370. P. 236–243. doi: 10.1016/j.ijcard.2022.11.010Luo W, Wei N, Sun Z, Gong Y. Association between serum α-klotho level and the prevalence of heart failure in the general population. Cardiovasc J Afr. 2023;(34):1–6. doi: 10.5830/CVJA-2023-042. Epub ahead of print.Luo W., Wei N., Sun Z., Gong Y. Association between serum α-klotho level and the prevalence of heart failure in the general population // Cardiovasc J Afr. 2023. N 34. P. 1–6. doi: 10.5830/CVJA-2023-042. Epub ahead of print.Mora-Fernández C, Pérez A, Mollar A, et al. Short-term changes in klotho and FGF23 in heart failure with reduced ejection fraction-a substudy of the DAPA-VO2 study. Front Cardiovasc Med. 2023;(10):1242108. doi: 10.3389/fcvm.2023.1242108Mora-Fernandez C., Perez A., Mollar A., et al. Short-term changes in klotho and FGF23 in heart failure with reduced ejection fraction-a substudy of the DAPA-VO2 study // Front Cardiovasc Med. 2023. N 10. P. 1242108. doi: 10.3389/fcvm.2023.1242108Nakano T, Kishimoto H, Tokumoto M. Direct and indirect effects of fibroblast growth factor 23 on the heart. Front Endocrinol (Lausanne). 2023;(14):1059179. doi: 10.3389/fendo.2023.1059179Nakano T., Kishimoto H., Tokumoto M. Direct and indirect effects of fibroblast growth factor 23 on the heart // Front Endocrinol (Lausanne). 2023. N 14. P. 1059179. doi: 10.3389/fendo.2023.1059179Agoro R, White KE. Regulation of FGF23 production and phosphate metabolism by bone-kidney interactions. Nat Rev Nephrol. 2023;19(3):185–193. doi: 10.1038/s41581-022-00665-xAgoro R., White K. Regulation of FGF23 production and phosphate metabolism by bone-kidney interactions // Nat Rev Nephrol. 2023. Vol. 19, N 3. P. 185–193. doi: 10.1038/s41581-022-00665-xGarcia-Fernandez N, Lavilla J, Martín PL, et al. Increased Fibroblast Growth Factor 23 in Heart Failure: Biomarker, Mechanism, or Both? Am J Hypertens. 2019;32(1):15–17. doi: 10.1093/ajh/hpy153Garcia-Fernandez N., Lavilla J., Martín P., et al. Increased fibroblast growth factor 23 in heart failure: biomarker, mechanism, or both? // Am J Hypertens. 2019. Vol. 32, N 1. P. 15–17. doi: 10.1093/ajh/hpy153Ho BB, Bergwitz C. FGF23 signalling and physiology. J Mol Endocrinol. 2021;66(2):R23–R32. doi: 10.1530/JME-20-0178Ho B., Bergwitz C. FGF23 signalling and physiology // J Mol Endocrinol. 2022. Vol. 66, N 2. P. R23–R32. doi: 10.1530/JME-20-0178Suzuki Y, Kuzina E, An SJ, et al. FGF23 contains two distinct high-affinity binding sites enabling bivalent interactions with α-Klotho. Proc Natl Acad Sci U S A. 2020;117(50):31800–31807. doi: 10.1073/pnas.2018554117Suzuki Y., Kuzina E., An S., et al. FGF23 contains two distinct high-affinity binding sites enabling bivalent interactions with α-Klotho // Proc Natl Acad Sci U S A. 2020. Vol. 117, N 50. P. 31800–31807. doi: 10.1073/pnas.2018554117Cipriani C, Minisola S, Colangelo L, et al. FGF23 functions and disease. Minerva Endocrinol (Torino). 2022;47(4):437–448. doi: 10.23736/S2724-6507.21.03378-2Cipriani C., Minisola S., Colangelo L., et al. FGF23 functions and disease // Minerva Endocrinol (Torino). 2022. Vol. 47, N 4. P. 437–448. doi: 10.23736/S2724-6507.21.03378-2Dastghaib S, Koohpeyma F, Shams M, et al. New concepts in regulation and function of the FGF23. Clin Exp Med. 2023;23(4):1055–1066. doi: 10.1007/s10238-022-00844-xDastghaib S., Koohpeyma F., Shams M., et al. New concepts in regulation and function of the FGF23 // Clin Exp Med. 2023. Vol. 23, N 4. P. 1055–1066. doi: 10.1007/s10238-022-00844-xLeifheit-Nestler M, Haffner D. Paracrine Effects of FGF23 on the Heart. Front Endocrinol (Lausanne). 2018;(9):278. doi: 10.3389/fendo.2018.00278Leifheit-Nestler M., Haffner D. Paracrine Effects of FGF23 on the Heart // Front Endocrinol (Lausanne). 2018. N 9. P. 278. doi: 10.3389/fendo.2018.00278Grabner A, Amaral AP, Schramm K, et al. Activation of Cardiac Fibroblast Growth Factor Receptor 4 Causes Left Ventricular Hypertrophy. Cell Metab. 2015;22(6):1020–1032. doi: 10.1016/j.cmet.2015.09.002Grabner A., Amaral A., Schramm K., et al. Activation of Cardiac Fibroblast Growth Factor Receptor 4 Causes Left Ventricular Hypertrophy // Cell Metab. 2015. Vol. 22, N 6. P. 1020–1032. doi: 10.1016/j.cmet.2015.09.002Liu M, Xia P, Tan Z, et al. Fibroblast growth factor-23 and the risk of cardiovascular diseases and mortality in the general population: A systematic review and dose-response meta-analysis. Front Cardiovasc Med. 2022;(9):989574. doi: 10.3389/fcvm.2022.989574Liu M., Xia P., Tan Z., et al. Fibroblast growth factor-23 and the risk of cardiovascular diseases and mortality in the general population: A systematic review and dose-response meta-analysis // Front Cardiovasc Med. 2022. N 9. P. 989574. doi: 10.3389/fcvm.2022.989574Vergaro G, Del Franco A, Aimo A, et al. Intact fibroblast growth factor 23 in heart failure with reduced and mildly reduced ejection fraction. BMC Cardiovasc Disord. 2023;23(1):433. doi: 10.1186/s12872-023-03441-2Vergaro G., Del Franco A., Aimo A., et al. Intact fibroblast growth factor 23 in heart failure with reduced and mildly reduced ejection fraction // BMC Cardiovasc Disord. 2023. Vol. 23, N 1. P. 433. doi: 10.1186/s12872-023-03441-2von Jeinsen B, Sopova K, Palapies L, et al. Bone marrow and plasma FGF-23 in heart failure patients: novel insights into the heart-bone axis. ESC Heart Fail. 2019;6(3):536–544. doi: 10.1002/ehf2.12416von Jeinsen B., Sopova K., Palapies L., et al. Bone marrow and plasma FGF-23 in heart failure patients: novel insights into the heart-bone axis // ESC Heart Fail. 2019. Vol. 6, N 3. P. 536–544. doi: 10.1002/ehf2.12416Elzayat RS, Bahbah WA, Elzaiat RS, Elgazzar BA. Fibroblast growth factor 23 in children with or without heart failure: a prospective study. BMJ Paediatr Open. 2023;7(1):e001753. doi: 10.1136/bmjpo-2022-001753Elzayat R., Bahbah W., Elzaiat R., Elgazzar B. Fibroblast growth factor 23 in children with or without heart failure: a prospective study // BMJ Paediatr Open. 2023. Vol. 7, N 1. P. e001753. doi: 10.1136/bmjpo-2022-001753Roy C, Lejeune S, Slimani A, et al. Fibroblast growth factor 23: a biomarker of fibrosis and prognosis in heart failure with preserved ejection fraction. ESC Heart Fail. 2020;7(5):2494–2507. doi: 10.1002/ehf2.12816Roy C., Lejeune S., Slimani A., et al. Fibroblast growth factor 23: a biomarker of fibrosis and prognosis in heart failure with preserved ejection fraction // ESC Heart Fail. 2020. Vol. 7, N 5. P. 2494–2507. doi: 10.1002/ehf2.12816Hofer F, Hammer A, Pailer U, et al. Relationship of Fibroblast Growth Factor 23 With Hospitalization for Heart Failure and Cardiovascular Outcomes in Patients Undergoing Cardiac Surgery. J Am Heart Assoc. 2023;12(5):e027875. doi: 10.1161/JAHA.122.027875Hofer F., Hammer A., Pailer U., et al. Relationship of Fibroblast Growth Factor 23 With Hospitalization for Heart Failure and Cardiovascular Outcomes in Patients Undergoing Cardiac Surgery // J Am Heart Assoc. 2023. Vol. 12, N 5. P. 027875. doi: 10.1161/JAHA.122.027875Binnenmars SH, Hoogslag GE, Yeung SMH, et al. Fibroblast Growth Factor 23 and Risk of New Onset Heart Failure With Preserved or Reduced Ejection Fraction: The PREVEND Study. J Am Heart Assoc. 2022;11(15):e024952. doi: 10.1161/JAHA.121.024952Binnenmars S., Hoogslag G., Yeung S., et al. Fibroblast Growth Factor 23 and Risk of New Onset Heart Failure with Preserved or Reduced Ejection Fraction: The PREVEND Study // J Am Heart Assoc. 2022. Vol. 11, N 15. P. e024952. doi: 10.1161/JAHA.121.024952Oniszczuk A, Kaczmarek A, Kaczmarek M, et al. Sclerostin as a biomarker of physical exercise in osteoporosis: A narrative review. Front Endocrinol (Lausanne). 2022;(13):954895. doi: 10.3389/fendo.2022.954895Oniszczuk A., Kaczmarek A., Kaczmarek M., et al. Sclerostin as a biomarker of physical exercise in osteoporosis: A narrative review // Front Endocrinol (Lausanne). 2022. N 13. P. 954895. doi: 10.3389/fendo.2022.954895Jaśkiewicz Ł, Chmielewski G, Kuna J, et al. The Role of Sclerostin in Rheumatic Diseases: A Review. J Clin Med. 2023;12(19):6248. doi: 10.3390/jcm12196248Jaśkiewicz Ł., Chmielewski G., Kuna J., et al. The Role of Sclerostin in Rheumatic Diseases: A Review // J Clin Med. 2023. Vol. 12, N 19. P. 6248. doi: 10.3390/jcm12196248Sanabria-de la Torre R, González-Salvatierra S, García-Fontana C, et al. Exploring the Role of Sclerostin as a Biomarker of Cardiovascular Disease and Mortality: A Scoping Review. Int J Environ Res Public Health. 2022;19(23):15981. doi: 10.3390/ijerph192315981Sanabria-de la Torre R., González-Salvatierra S., Garcia-Fontana C., et al. Exploring the Role of Sclerostin as a Biomarker of Cardiovascular Disease and Mortality: A Scoping Review // Int J Environ Res Public Health. 2022. Vol. 19, N 23. P. 15981. doi: 10.3390/ijerph192315981Vasiliadis ES, Evangelopoulos DS, Kaspiris A, et al. Sclerostin and Its Involvement in the Pathogenesis of Idiopathic Scoliosis. J Clin Med. 2021;10(22):5286. doi: 10.3390/jcm10225286Vasiliadis E., Evangelopoulos D., Kaspiris A., et al. Sclerostin and Its Involvement in the Pathogenesis of Idiopathic Scoliosis // J Clin Med. 2021. Vol. 10, N 22. P. 5286. doi: 10.3390/jcm10225286Maeda K, Kobayashi Y, Koide M, et al. The Regulation of Bone Metabolism and Disorders by Wnt Signaling. Int J Mol Sci. 2019;20(22):5525. doi: 10.3390/ijms20225525Maeda K., Kobayashi Y., Koide M., et al. The Regulation of Bone Metabolism and Disorders by Wnt Signaling // Int J Mol Sci. 2019. Vol. 20, N 22. P. 5525. doi: 10.3390/ijms20225525Tu X, Delgado-Calle J, Condon KW, et al. Osteocytes mediate the anabolic actions of canonical Wnt/β-catenin signaling in bone. Proc Natl Acad Sci U S A. 2015;112(5):E478–E486. doi: 10.1073/pnas.1409857112Tu X., Delgado-Calle J., Condon K.W., et al. Osteocytes mediate the anabolic actions of canonical Wnt/β-catenin signaling in bone // Proc Natl Acad Sci U S A. 2015. Vol. 112, N 5. P. E478–E486. doi: 10.1073/pnas.1409857112Daniele G, Winnier D, Mari A, et al. Sclerostin and Insulin Resistance in Prediabetes: Evidence of a Cross Talk Between Bone and Glucose Metabolism. Diabetes Care. 2015;38(8):1509–1517. doi: 10.2337/dc14-2989Daniele G., Winnier D., Mari A., et al. Sclerostin and Insulin Resistance in Prediabetes: Evidence of a Cross Talk Between Bone and Glucose Metabolism // Diabetes Care. 2015. Vol. 38, N 8. P. 1509–1517. doi: 10.2337/dc14-2989Matsui S, Yasui T, Kasai K, et al. Increase in circulating sclerostin at the early stage of menopausal transition in Japanese women. Maturitas. 2016;(83):72–77. doi: 10.1016/j.maturitas.2015.10.001Matsui S., Yasui T., Kasai K., et al. Increase in Circulating Sclerostin at the Early Stage of Menopausal Transition in Japanese Women // Maturitas. 2016. N 83. P. 72–77. doi: 10.1016/j.maturitas.2015.10.001Mackey RH, Venkitachalam L, Sutton-Tyrrell K. Calcifications, arterial stiffness and atherosclerosis. Adv Cardiol. 2007;(44):234–244. doi: 10.1159/000096744Mackey R., Venkitachalam L., Sutton-Tyrrell K. Calcifications, Arterial Stiffness and Atherosclerosis// Adv Cardiol. 2007. N 44. P. 234–244. doi: 10.1159/000096744Sabancilar I, Unsal V, Demir F, et al. Does oxidative status affect serum sclerostin levels in patients with type 2 diabetes mellitus? Folia Med (Plovdiv). 2023;65(1):46–52. doi: 10.3897/folmed.65.e72953Sabancilar I., Unsal V., Demir F., et al. Does oxidative status affect serum sclerostin levels in patients with type 2 diabetes mellitus? // Folia Med (Plovdiv). 2023. Vol. 65, N 1. P. 46–52. doi: 10.3897/folmed.65.e72953Golledge J, Thanigaimani S. Role of Sclerostin in Cardiovascular Disease. Arterioscler Thromb Vasc Biol. 2022;42(7):e187–e202. doi: 10.1161/ATVBAHA.122.317635Golledge J., Thanigaimani S. Role of sclerostin in cardiovascular disease // Arterioscler Thromb Vasc Biol. 2022. Vol. 42, N 7. P. e187–e202. doi: 10.1161/ATVBAHA.122.317635Frysz M, Gergei I, Scharnagl H, et al. Circulating Sclerostin Levels Are Positively Related to Coronary Artery Disease Severity and Related Risk Factors. J Bone Miner Res. 2022;37(2):273–284. doi: 10.1002/jbmr.4467Frysz M., Gergei I., Scharnagl H., et al. Circulating Sclerostin Levels Are Positively Related to Coronary Artery Disease Severity and Related Risk Factors // J Bone Miner Res. 2022. Vol. 37, N 2. P. 273–284. doi: 10.1002/jbmr.4467