ФАКТОР РОСТА ФИБРОБЛАСТОВ-23 (FGF23) – НОВЫЙ БИОЛОГИЧЕСКИЙ МАРКЕР ПРИ СЕРДЕЧНОЙ НЕДОСТАТОЧНОСТИ
Обзорная статья
Дата публикации: апреля 26, 2022
Ключевые слова
биологические маркеры
сердечная недостаточность
фактор роста фибробластов 23
сердечная недостаточность
фактор роста фибробластов 23
Как цитировать
[1]
А. М. Алиева, Т. В. Пинчук, В. А. Кисляков, Р. К. Валиев, Р. А. Аракелян, и И. Г. Никитин, ФАКТОР РОСТА ФИБРОБЛАСТОВ-23 (FGF23) – НОВЫЙ БИОЛОГИЧЕСКИЙ МАРКЕР ПРИ СЕРДЕЧНОЙ НЕДОСТАТОЧНОСТИ, КМКВ, вып. 1, сс. 59-65, апр. 2022.
Аннотация
В настоящее время фактор роста фибробластов 23 (FGF23) является одним из исследуемых биологических маркеров при сердечной недостаточности. Уровень FGF23 обычно анализируется как важный маркер для диагностики и оценки прогноза у пациентов с хронической болезнью почек. Было показано, что концентрация FGF23 в плазме крови значимо увеличивается по мере утяжеления хронической болезни почек, более того, она независимо связана с неблагоприятным исходом как у недиализных пациентов, так и у больных, получающих заместительную почечную терапию. Недавний систематический обзор и метаанализ 10 проспективных исследований (5 в общей популяции, 4 у пациентов с хронической болезнью почек, не нуждающихся в заместительной почечной терапии, и 1 у больных, находящихся на диализе), продемонстрировал связь между FGF23 и риском развития сердечной недостаточности. Роль FGF23 при заболеваниях сердца в настоящее время все еще непонятна, особенно эффекты, связанные не только со структурными изменениями в миокарде, но и с сердечной дисфункцией. Высокие циркулирующие уровни FGF23 были связаны с гипертрофией левого желудочка, эндотелиальной дисфункцией и атеросклерозом. Кроме того, остается неясным, играет ли FGF23 негативную роль в развитии неблагоприятных сердечно-сосудистых событий или высокие его показатели в крови являются следствием нарушений функций сердца. Необходимо дальнейшее более глубинное понимание роли FGF23, а также будущие клинические исследования для определения диагностической, прогностической и, возможно, даже терапевтической значимости этого биологического маркера.Литература
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2. Mozaffarian D. et al. Heart disease and stroke statistics –2016 update: a report from the American Heart Association // Circulation. – 2016. – V. 133. – № 4. – P. e38–e360.
3. Терещенко С.Н. и др. Хроническая сердечная недостаточность. Клинические рекомендации 2020 // Российский кардиологический журнал. – 2020. – № 11. – C. 311–374. [Tereshchenko S.N. et al. 2020 Clinical practice guidelines for chronic heart failure // Russian Journal of Cardiology.– 2020. – № 11. – P. 311–374. In Russian].
4. Ziaeian B., Fonarow G.C. Epidemiology and aetiology of heart failure // Nat Rev Cardiol. – 2016. – V. 13. – № 6. – P. 368–378.
5. Taylor C.J. et al. Trends in survival after a diagnosis of heart failure in the United Kingdom 2000–2017: population based cohort study // BMJ. – 2019. – V. 364. – P. l223.
6. Гаспарян А.Ж., Шлевков Н.Б., Скворцов А.А. Возможности современных биомаркеров для оценки риска развития желудочковых тахиаритмий и внезапной сердечной смерти у больных хронической сердечной недостаточностью // Кардиология. – 2020. – T. 60. – № 4. – C. 101–108. [Gasparyan A.Z., Shlevkov N.B., Skvortsov A.A. Possibilities of modern biomarkers for assessing the risk of developing ventricular tachyarrhythmias and sudden cardiac death in patients with chronic heart failure // Kardiologiia. – 2020. – V. 60. – № 4. – P. 101–108. In Russian].
7. Алиева А.М. и др. Клиническое значение определения биомаркеров крови у больных с хронической сердечной недостаточностью // Архив внутренней медицины. – 2018. – Т. 8. – № 5. – C. 333–345. [Aliyeva A.M. et al. Clinical value of blood biomarkers in patients with chronic heart failure // The Russian Archives of Internal Medicine. – 2018. – V. 8. – № 5. – P. 333–345. In Russian].
8. Алиева А.М. и др. Клиническое значение определения биомаркера крови ST2 у больных с хронической сердечной недостаточностью // Consilium Medicum. – 2021. – Т. 23. – № 6. – С. 522–526. [Alieva A.M. et al. Сlinical value of blood biomarker ST2 in patients with chronic heart failure // Consilium Medicum. – 2021. – V. 23. – № 6. – P. 522–526. In Russian].
9. Itoh N., Ornitz D.M. Evolution of the Fgf and Fgfr gene families // Trends Genets. – 2004. – V. 20. – № 11. – P. 563–569.
10. Алиева А.М. и др. Фракталкин и сердечно-сосудистые заболевания // Consilium Medicum. – 2020. – Т. 22. – № 5. [Alieva A.M. et al. Fractalkin and cardiovascular disease // Consilium Medicum. – 2020. – V. 22. – № 5. In Russian].
11. Brewer J.R., Mazot P., Soriano P. Genetic insights into the mechanisms of Fgf signaling // Genes Dev. – 2016. – V. 30. – № 7. – P. 751–771.
12. Spivak-Kroizman T. et al. Heparin-induced oligomerization of FGF molecules is responsible for FGF receptor dimerization, activation, and cell proliferation // Cell. – 1994. – V. 79. – № 6. – P. 1015–1024.
13. Leifheit-Nestler M., Haffner D. Paracrine effects of FGF23 on the heart // Front Endocrinol. – 2018. – V. 9. – P. 278.
14. Urakawa I. et al. Klotho converts canonical FGF receptor into a specific receptor for FGF23 // Nature. – 2006. – V. 444. – № 7120. – P. 770–774.
15. Melnik A. Protein Klotho and FGF23 fibroblasts growth factor as markers of chronic renal disease // Kidneys. – 2017. – V. 6. – № 3. – Р. 132–138.
16. Garcia-Fernandez N. et al. Increased fibroblast growth factor 23 in heart failure: biomarker, mechanism, or both? // Am J Hypertens. – 2019. – V. 32. – № 1. – P. 15–17.
17. Martin A., David V., Quarles L.D. Regulation and function of the FGF23/klotho endocrine pathways // Physiol Rev. – 2012. – V. 92. – № 1. – P. 131–155.
18. Andrukhova O. et al. FGF23 regulates renal sodium handling and blood pressure // EMBO Mol Med. – 2014. – V. 6. – № 6. – P. 744–759.
19. Erben R.G., Andrukhova O. FGF23 regulation of renal tubular solute transport // Curr Opin Nephrol Hypertens. – 2015. – V. 24. – № 5. – P. 450–456.
20. Bao J.F. et al. A land of controversy: fibroblast growth factor-23 and uremic cardiac hypertrophy // J Am Soc Nephrol. – 2020. – V. 31. – № 7. – P. 1423–1434.
21. Rodelo-Haad C. et al. FGF23, biomarker or target? // Toxins. – 2019. – V. 11. – № 3. – P. 175.
22. ADHR Consortium. Autosomal dominant hypophosphataemic rickets is associated with mutations in FGF23 // Nat Genet. – 2000. – V. 26. – № 3. – P. 345–348.
23. Blau J.E., Collins M.T. The PTH-Vitamin D-FGF23 axis // Rev Endocr Metab Disord. – 2015. – V. 16. – № 2. – P. 165–174.
24. Navarro‐García J.A. et al. PTH, vitamin D, and the FGF‐23–klotho axis and heart: going beyond the confines of nephrology // Eur J Clin Invest. – 2018. – V. 48. – № 4. – P. e12902.
25. Милованова Л.Ю. и др. Нарушение соотношения сывороточных уровней фактора роста фибробластов-23 (FGF-23)/растворимой формы белка Клото (sKlotho)/гликопротеина склеростина –новый маркер поражения сердечно-сосудистой системы у больных хронической болезнью почек, получающих лечение ГД или ГДФ // Терапевтический архив. – 2018. – Т. 90. – № 6. – C. 48–54. [Milovanova L.Yu. et al. Violation of the ratio of serum levels of fibroblast growth factor-23 (FGF-23)/soluble protein Klotho (sKlotho)/glycoprotein sclerostin is a new marker of cardiovascular damage in patients with chronic kidney disease receiving treatment with HD or HDF // Therapeutic archive. – 2018. – V. 90. – № 6. – P. 48–54. In Russian].
26. Mathew J.S. et al. Fibroblast growth factor-23 and incident atrial fibrillation: the Multi-Ethnic Study of Atherosclerosis (MESA) and the Cardiovascular Health Study (CHS) // Circulation. – 2014. – V. 130. – № 4. – P. 298–307.
27. Larsson T. et al. Circulating concentration of FGF23 increases as renal function declines in patients with chronic kidney disease, but does not change in response to variation in phosphate intake in healthy volunteers // Kidney Int. – 2003. – V. 64. – № 6. – P . 2272–2279.
28. De Borst M.H. et al. Cross talk between the renin-angiotensin-aldosterone system and vitamin D-FGF-23-klotho in chronic kidney disease // J Am Soc Nephrol. – 2011. – V. 22. – № 9. – P. 1603–1609.
29. Marthi A. et al. Fibroblast growth factor-23 and risks of cardiovascular and noncardiovascular diseases: a meta-analysis // J Am Soc Nephrol. – 2018. – V. 29. – № 7. – P. 2015–2027.
30. Lutsey P.L. et al. Fibroblast growth factor‐23 and incident coronary heart disease, heart failure, and cardiovascular mortality: the Atherosclerosis Risk in Communities study // J Am Heart Assoc. – 2014. – V. 3. – № 3. – P. e000936.
31. Vázquez-Sánchez S. et al. An overview of FGF23 as a novel candidate biomarker of cardiovascular risk // Front Physiol. – 2021. – V. 12. – P. 632260.
32. Kestenbaum B. et al. Fibroblast growth factor-23 and cardiovascular disease in the general population: the Multi-Ethnic Study of Atherosclerosis // Circ Heart Fail. – 2014. – V. 7. – № 3. – P. 409–417.
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