Preview

Russian Journal of Cardiology

Advanced search

Biomarkers of myocardial fibrosis and their genetic regulation in patients with heart failure

https://doi.org/10.15829/1560-4071-2020-3933

Abstract

Currently, the development of chronic heart failure (CHF) is considered from the perspective of pathological structural remodeling of myocardium and fibrosis. Despite the widespread use of molecular genetic markers in clinical practice, only a small number of them are used to evaluate remodeling processes, as well as to predict potential complications associated with heart failure (HF). In addition, the relationship between many biomarkers with instrumental and histological confirmation of myocardial fibrosis has not yet been determined. Myocardial fibrosis remains quite debatable and controversial subject, which actualizes the further study of this direction. The discovery of pathogenetic and diagnostic markers of myocardial fibrosis could contribute to the development of targeted therapy. Of particular interest is the search for possible pathogenetic markers, since this is relevant for clinical practice.

About the Authors

T. B. Pecherina
Research Institute for Complex Issues of Cardiovascular Diseases
Russian Federation
Kemerovo


A. G. Kutikhin
Research Institute for Complex Issues of Cardiovascular Diseases
Russian Federation
Kemerovo


References

1. GBD 2017 Causes of Death Collaborators. Global, regional, and national age-sex-specific mortality for 282 causes of death in 195 countries and territories, 1980-2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet. 2018;392(10159):1736-1788. doi: 10.1016/S0140-6736(18)32203-7.

2. Ferreira JP, Krausy S, Mitchellz S et al. World Heart Federation Roadmap for Heart Failure. GLOBAL HEART. 2019;14(3):197-214. Doi: 10.1016/j.gheart.2019.07.004.

3. Benjamin EJ, Virani SS, Callaway CW, et al. American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee. Heart Disease and Stroke Statistics-2018 Update: A Report From the American Heart Association. Circulation. 2018;137(12):e67-e492. Doi: 10.1161/CIR.0000000000000558.

4. Bloom MW, Greenberg B, Jaarsma T, J et al. Heart failure with reduced ejection fraction. Nat Rev Dis Primers. 2017;3:17058. Doi: 10.1038/nrdp.2017.58.

5. Metra M, Teerlink JR. Heart failure. Lancet. 2017;390(10106):1981-1995. Doi: 10.1016/S0140-6736(17)31071-1.

6. Bing R., Dwec M.R. Myocardial fibrosis: why image, how to image and clinical implications. Heart 2019;105:1832–1840. Doi:10.1136/heartjnl-2019-315560.

7. Leask A. Getting to the heart of the matter: new insights into cardiac fibrosis. Circ Res. 2015;116(7):1269-1276. Doi: 10.1161/CIRCRESAHA.116.305381.

8. Travers JG, Kamal FA, Robbins J, et al. Cardiac Fibrosis: The Fibroblast Awakens. Circ Res. 2016;118(6):1021-1040. Doi: 10.1161/CIRCRESAHA.115.306565.

9. Talman V, Ruskoaho H. Cardiac fibrosis in myocardial infarction-from repair and remodeling to regeneration. Cell Tissue Res. 2016;365(3):563-81. Doi: 10.1007/s00441-016-2431-9.

10. Tallquist MD. Cardiac Fibroblast Diversity Annu. Rev. Physiol. 2020;82:63-78. Doi: 10.1146/annurev-physiol-021119-034527

11. Tian J, An X, Niu L. Myocardial fibrosis in congenital and pediatric heart disease. Exp Ther Med. 2017;13(5):1660-1664. Doi: 10.3892/etm.2017.4224.

12. Jin L, Zhang J, Deng Z at al. Mesenchymal stem cells ameliorate myocardial fibrosis in diabetic cardiomyopathy via the secretion of prostaglandin E2. Stem Cell Research & Therapy. 2020; 11:122. Doi: 10.1186/s13287-020-01633-7

13. Humeres C, Frangogiannis NG. Fibroblasts in the Infarcted, Remodeling, and Failing Heart. JACC: Basic to Translational Science. 2019;4(3):449-467. Doi: 10.1016/j.jacbts.2019.02.006

14. Schüttler D, Clauss S, Weckbach LT at al. Molecular Mechanisms of Cardiac Remodeling and Regeneration in Physical Exercise. Cells 2019;8(10):1128. Doi: 10.3390/cells8101128

15. Li L, Zhao Q, Kong W. Extracellular matrix remodeling and cardiac fibrosis. Matrix Biol. 2018;68-69:490-506. Doi: 10.1016/j.matbio.2018.01.013.

16. Frangogiannis NG. Cardiac fibrosis: Cell biological mechanisms, molecular pathways and therapeutic opportunities. Mol Aspects Med. 2018;65:70-99. Doi: 10.1016/j.mam.2018.07.001.

17. Fraccarollo D, Galuppo P, Bauersachs J, et al. Collagen accumulation after myocardial infarction: effects of ETA receptor blockade and implications for early remodeling. Cardiovasc Res. 2002;54(3):559-567. Doi: 10.1016/S0008-6363(02)00256-0

18. Pan X, Chen Z, Huang R, et al. Transforming growth factor β1 induces the expression of collagen type I by DNA methylation in cardiac fibroblasts. PLoS One. 2013;8(4):e60335. Doi: 10.1371/journal.pone.0060335.

19. Dobaczewski M, Bujak M, Li N, et al. Smad3 signaling critically regulates fibroblast phenotype and function in healing myocardial infarction. Circ Res. 2010;107(3):418-428. Doi: 10.1161/CIRCRESAHA.109.216101.

20. Koshman YE, Patel N, Chu MS, et al. Regulation of connective tissue growth factor gene expression and fibrosis in human heart failure. J Card Fail. 2013;19(4):283-294. Doi: 10.1016/j.cardfail.2013.01.013

21. Chi H, Feng H, Shang X. Circulating Connective Tissue Growth Factor Is Associated with Diastolic Dysfunction in Patients with Diastolic Heart Failure. Cardiology 2019;143:77–84. Doi:10.1159/000499179.

22. Vainio LE, Szabó Z, Lin R et al. Connective Tissue Growth Factor Inhibition Enhances Cardiac Repair and Limits Fibrosis After Myocardial Infarction. J Am Coll Cardiol Basic Trans Science. 2019;4(1):83–94. Doi: 10.1016/j.jacbts.2018.10.007.

23. Zhang N, Wei W-Y, Li L-L at al. Therapeutic Potential of Polyphenols in Cardiac Fibrosis. Front. Pharmacol. 2018; 9(122):1-15. doi: 10.3389/fphar.2018.00122

24. Chen XQ, Liu X, Wang QX, et al. Pioglitazone inhibits angiotensin II-induced atrial fibroblasts proliferation via NF-kB/TGF-β1/TRIF/TRAF6 pathway. Exp Cell Res. 2015;330(1):43-55. doi: 10.1016/j.yexcr.2014.08.021

25. Ma ZG, Yuan YP, Wu HM at al. Cardiac fibrosis: new insights into the pathogenesis. Int J Biol Sci 2018; 14(12):1645-1657. Doi:10.7150/ijbs.28103.

26. Weng X, Yu L, Liang P, et al. Endothelial MRTF-A mediates angiotensin II induced cardiac hypertrophy. J Mol Cell Cardiol. 2015;80:23-30. Doi:10.1016/j.yjmcc.2014.11.009.

27. Murphy SP, Kakkar R, Cian P. McCarthy at al. Inflammation in Heart Failure. J Am Coll Cardiol. 2020.75(11): 1324-1340. Doi: 10.1016/j.jacc.2020.01.014.

28. Steen EH, Wang X, Balaji S et al. The Role of the Anti-Inflammatory Cytokine Interleukin-10 in Tissue Fibrosis. Adv Wound Care (New Rochelle). 2020;9(4):184–198. DOI: 10.1089/wound.2019.1032

29. Yue Y, Huang S, Wang L et al. M2b Macrophages Regulate Cardiac Fibroblast Activation and Alleviate Cardiac Fibrosis After Reperfusion Injury. Circ J. 2020; 84(4):626-635. Doi: 10.1253/circj.CJ-19-0959.

30. Herrera J, Henke CA, Bitterman PB. Extracellular matrix as a driver of progressive Fibrosis. J Clin Invest. 2018;128(1):45-53. Doi:10.1172/JCI93557.

31. Taha IN, Naba A. Exploring the extracellular matrix in health and disease using proteomics. Essays Biochem. 2019;63(3):417–432. Doi: 10.1042/EBC20190001

32. Ruddy JM, Ikonomidis JS, Jones JA. Multidimensional Contribution of Matrix Metalloproteinases to Atherosclerotic Plaque Vulnerability: Multiple Mechanisms of Inhibition to Promote Stability. J Vasc Res. 2016;53(1-2):1-16. Doi: 10.1159/000446703.

33. Johnson JL. Metalloproteinases in atherosclerosis. Eur J Pharmacol. 2017;816:93-106. Doi: 10.1016/j.ejphar.2017.09.007.

34. Nong Z, O'Neil C, Lei M, et al. Type I collagen cleavage is essential for effective fibrotic repair after myocardial infarction. Am J Pathol. 2011;179(5):2189-2198. Doi: 10.1016/j.ajpath.2011.07.017.

35. Nagalingama RS., Safib HA, Al-Hattaba DS at al. Regulation of cardiac fibroblast MMP2 gene expression by scleraxis. 2018;120:64-73. Doi: 10.1016/j.yjmcc.2018.05.004.

36. DeLeon-Pennell KY, Tian Y, Zhang B, et al. CD36 Is a Matrix Metalloproteinase-9 Substrate That Stimulates Neutrophil Apoptosis and Removal During Cardiac Remodeling. Circ Cardiovasc Genet. 2016;9(1):14-25. Doi: 10.1161/CIRCGENETICS.115.00124

37. Münch J, Avanesov M, Bannas P, et al. Serum Matrix Metalloproteinases as Quantitative Biomarkers for Myocardial Fibrosis and Sudden Cardiac Death Risk Stratification in Patients With Hypertrophic Cardiomyopathy. J Card Fail. 2016;22(10):845-850. Doi: 10.1016/j.cardfail.2016.03.010.

38. Takawale A, Zhang P, Patel VB, et al. Tissue Inhibitor of Matrix Metalloproteinase-1 Promotes Myocardial Fibrosis by Mediating CD63-Integrin β1 Interaction. Hypertension. 2017;69(6):1092-1103. Doi: 10.1161/HYPERTENSIONAHA.117.09045.

39. Liu Y, Xiao Y, Liu J, et al. Copper-induced reduction in myocardial fibrosis is associated with increased matrix metalloproteins in a rat model of cardiac hypertrophy. Metallomics. 2018;10(1):201-208. Doi: 10.1039/c7mt00165g.

40. Park S., Nguyen N.B., Pezhouman A. at al. Cardiac fibrosis: potential therapeutic targets. Transl Res. 2019; 209:121-137. Doi: 10.1016/j.trsl.2019.03.001.

41. Fan Z, Guan J. Antifibrotic therapies to control cardiac fibrosis. Biomater Res. 2016;20:13. Doi: 10.1186/s40824-016-0060-8.

42. López B, González A, Ravassa S, et al. Circulating Biomarkers of Myocardial Fibrosis: The Need for a Reappraisal. J Am Coll Cardiol. 2015;65(22):2449-2456. Doi: 10.1016/j.jacc.2015.04.026.

43. Schimmel K., Jung M., Foinquinos A. at. al. Natural Compound Library Screening Identifies New Molecules for the Treatment of Cardiac Fibrosis and Diastolic Dysfunction. Circulation. 2020; 141:751–767. Doi: 10.1161/CIRCULATIONAHA.119.042559.

44. Kockova R, Kacer P, Pirk J, et al. Native T1 Relaxation Time and Extracellular Volume Fraction as Accurate Markers of Diffuse Myocardial Fibrosis in Heart Valve Disease - Comparison With Targeted Left Ventricular Myocardial Biopsy. Circ J. 2016;80(5):1202-1209. Doi: 10.1253/circj.CJ-15-1309.

45. Liu CY, Heckbert SR, Lai S et al. Association of Elevated NT-proBNP With Myocardial Fibrosis in the Multi-Ethnic Study of Atherosclerosis (MESA). J Am Coll Cardiol. 2017;70(25):3102-3109. Doi: 10.1016/j.jacc.2017.10.044.

46. Lurz JA, Luecke C, Lang D, et al. CMR-Derived Extracellular Volume Fraction as a Marker for Myocardial Fibrosis: The Importance of Coexisting Myocardial Inflammation. JACC Cardiovasc Imaging. 2018;11(1):38-45. Doi: 10.1016/j.jcmg.2017.01.025.

47. Inozemtseva AA, Kashtalap VV, Gordeeva LA et al. Association gene APOE with clinical and anamnestic characteristics of severity ST-segment elevation myocardial infarction. Complex Issues of Cardiovascular Diseases. 2016;(4):59-65. (In Russ.) . Doi: 10.17802/2306-1278-2016-4-59-65.

48. Barbarash OL, Gruzdeva OV, Pecherina TB et al. Predictors of myocardial fibrosis and loss of epicardial adipose tissue volume in the long-term period after myocardial infarction. Russian Journal of Cardiology. 2020;25 (2): 31-40. (In Russ.) Doi:10.15829/1560-4071-2020-2-3474.


Review

For citations:


Pecherina T.B., Kutikhin A.G. Biomarkers of myocardial fibrosis and their genetic regulation in patients with heart failure. Russian Journal of Cardiology. 2020;25(10):3933. (In Russ.) https://doi.org/10.15829/1560-4071-2020-3933

Views: 1351


Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.


ISSN 1560-4071 (Print)
ISSN 2618-7620 (Online)