4.5 Review

Galectin-3: A Modifiable Risk Factor in Heart Failure

期刊

CARDIOVASCULAR DRUGS AND THERAPY
卷 28, 期 3, 页码 237-246

出版社

SPRINGER
DOI: 10.1007/s10557-014-6520-2

关键词

Galectin-3; Biomarker; Heart failure; Cardiac remodeling; Fibrosis

资金

  1. Abbott
  2. BG Medicine
  3. Netherlands Organisation for Scientific Research, NWO VIDI grant [917.13.350]
  4. AstraZeneca
  5. Biomerieux
  6. Pfizer
  7. Baxter
  8. Novartis
  9. Swiss National Science Foundation
  10. Swiss Heart Foundation
  11. Cardiovascular Research Foundation Basel
  12. Alere
  13. Brahms
  14. Critical Diagnostics
  15. Nanosphere
  16. Roche
  17. Siemens
  18. University Basel
  19. University Hospital Basel
  20. Bristol-Myers Squibb
  21. BRAHMS GmbH
  22. EU FP7 Programme
  23. Vifor Int.
  24. Medicines Company
  25. Cardiorentis
  26. Daiichi-Sankyo
  27. GE
  28. Janssen
  29. Lilly
  30. Singulex
  31. Verathon
  32. Roche Diagnostics
  33. EFG Diagnostics

向作者/读者索取更多资源

Myocardial galectin-3 is upregulated upon cardiac stressors such as angiotensin II and pressure overload leading to cardiac remodeling and heart failure. The expression level of galectin-3 mirrors the progression and severity of heart failure and therefore, galectin-3 is being used as a biomarker for heart failure. However, as galectin-3 is causally involved in pathological myocardial fibrosis it has been suggested that galectin-3 also actively contributes to heart failure development. In this review we discuss how galectin-3 could be a target for therapy in heart failure. Currently, attempts are being made to target or inhibit galectin-3 using natural or pharmaceutical inhibitors with the aim to ameliorate heart failure. Available experimental evidence suggests that galectin-3 inhibition indeed may represent a novel tool to treat heart failure. A strong interaction with aldosterone, another strong pro-fibrotic factor, has been described. Clinical studies are needed to prove if galectin-3 may be used to install specific treatment regimens.

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