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Nistri S, Sassoli C, Bani D. Notch Signaling in Ischemic Damage and Fibrosis: Evidence and Clues from the Heart. Front Pharmacol. 2017;8:187doi: 10.3389/fphar.2017.00187.
Nistri, S., Sassoli, C., & Bani, D. (2017). Notch Signaling in Ischemic Damage and Fibrosis: Evidence and Clues from the Heart. Frontiers in pharmacology, 8187. https://doi.org/10.3389/fphar.2017.00187
Nistri, Silvia, et al. "Notch Signaling in Ischemic Damage and Fibrosis: Evidence and Clues from the Heart." Frontiers in pharmacology vol. 8 (2017): 187. doi: https://doi.org/10.3389/fphar.2017.00187
Nistri S, Sassoli C, Bani D. Notch Signaling in Ischemic Damage and Fibrosis: Evidence and Clues from the Heart. Front Pharmacol. 2017 Apr 05;8:187. doi: 10.3389/fphar.2017.00187. eCollection 2017. PMID: 28424623; PMCID: PMC5381357.
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Front Pharmacol. 2017 Apr 05;8:187. doi: 10.3389/fphar.2017.00187. eCollection 2017.

Notch Signaling in Ischemic Damage and Fibrosis: Evidence and Clues from the Heart.

Frontiers in pharmacology

Silvia Nistri, Chiara Sassoli, Daniele Bani

Affiliations

  1. Research Unit of Histology and Embryology, Department of Experimental and Clinical Medicine, University of FlorenceFlorence, Italy.
  2. Department of Experimental and Clinical Medicine, Section of Anatomy and Histology, University of FlorenceFlorence, Italy.

PMID: 28424623 PMCID: PMC5381357 DOI: 10.3389/fphar.2017.00187

Abstract

Notch signaling is a major intercellular coordination mechanism highly conserved throughout evolution. In vertebrates, Notch signaling is physiologically involved in embryo development, including mesenchymal cell commitment, formation of heart tissues and angiogenesis. In post-natal life, Notch signaling is maintained as a key mechanism of cell-cell communication and its dysregulations have been found in pathological conditions such as ischemic and fibrotic diseases. In the heart, Notch takes part in the protective response to ischemia, being involved in pre- and post-conditioning, reduction of reperfusion-induced oxidative stress and myocardial damage, and cardiomyogenesis. Conceivably, the cardioprotective effects of Notch may depend on neo-angiogenesis, thus blunting lethal myocardial ischemia, as well as on direct stimulation of cardiac cells to increase their resistance to injury. Another post-developmental adaptation of Notch signaling is fibrosis: being involved in the orientation of mesenchymal cell fate, Notch can modulate the differentiation of pro-fibrotic myofibroblasts, e.g., by reducing the effects of the profibrotic cytokine TGF-β. In conclusion, Notch can regulate the interactions between heart muscle and stromal cells and switch cardiac repair from a pro-fibrotic default pathway to a pro-cardiogenic one. These features make Notch signaling a suitable target for new cardiotropic therapies.

Keywords: Notch; cardiac preconditioning; fibrosis; heart; ischemia-reperfusion

References

  1. Circ Res. 2014 Sep 12;115(7):636-49 - PubMed
  2. Pharmacol Res. 2016 Apr 21;108:57-64 - PubMed
  3. Circ Res. 2012 Jun 8;110(12):1628-45 - PubMed
  4. Exp Physiol. 2015 Jun;100(6):652-66 - PubMed
  5. Genes Dev. 2004 Jan 1;18(1):99-115 - PubMed
  6. Physiol Res. 2011;60(5):739-48 - PubMed
  7. Circ Res. 2011 Jan 7;108(1):51-9 - PubMed
  8. J Cell Mol Med. 2014 Mar;18(3):363-70 - PubMed
  9. Clin Genet. 2003 Dec;64(6):461-72 - PubMed
  10. Circ Res. 2008 May 9;102(9):1025-35 - PubMed
  11. Methods. 2014 Jun 15;68(1):173-82 - PubMed
  12. N Engl J Med. 2015 Mar 19;372(12):1138-49 - PubMed
  13. FASEB J. 2015 Jan;29(1):239-49 - PubMed
  14. Mol Ther. 2013 Oct;21(10):1841-51 - PubMed
  15. Cardiovasc Toxicol. 2016 Oct;16(4):316-24 - PubMed
  16. Am J Physiol Heart Circ Physiol. 2003 Aug;285(2):H579-88 - PubMed
  17. Eur Heart J. 2014 Aug 21;35(32):2140-5 - PubMed
  18. Basic Res Cardiol. 2013 Sep;108(5):373 - PubMed
  19. Cell. 2009 Apr 17;137(2):216-33 - PubMed
  20. Nat Rev Genet. 2008 Jan;9(1):49-61 - PubMed
  21. J Cell Biol. 2008 Oct 6;183(1):129-41 - PubMed
  22. Nat Med. 2003 Jun;9(6):669-76 - PubMed
  23. Drug Des Devel Ther. 2015 Aug 11;9:4599-611 - PubMed
  24. Circ Res. 2016 Feb 5;118(3):400-9 - PubMed
  25. Curr Mol Med. 2006 Dec;6(8):905-18 - PubMed
  26. PLoS One. 2013 May 21;8(5):e63896 - PubMed
  27. Circ Res. 2010 Feb 19;106(3):559-72 - PubMed
  28. Circ Res. 2016 Jan 8;118(1):e1-e18 - PubMed
  29. Proc Natl Acad Sci U S A. 2008 Oct 7;105(40):15529-34 - PubMed
  30. Angiogenesis. 2008;11(1):41-51 - PubMed
  31. Tissue Eng Part A. 2015 Sep;21(17-18):2315-22 - PubMed
  32. Expert Rev Cardiovasc Ther. 2016 Jun;14 (6):667-75 - PubMed
  33. Circ Res. 2016 Mar 18;118(6):1021-40 - PubMed
  34. Circulation. 2011 Mar 1;123(8):866-76 - PubMed
  35. J Transl Med. 2013 Oct 08;11:251 - PubMed
  36. Eur Heart J. 2014 Aug 21;35(32):2174-85 - PubMed
  37. Circ J. 2016 Oct 25;80(11):2269-2276 - PubMed
  38. Nat Rev Genet. 2012 Sep;13(9):654-66 - PubMed
  39. J Mol Cell Cardiol. 2011 Sep;51(3):399-408 - PubMed
  40. J Cell Sci. 2013 May 15;126(Pt 10):2135-40 - PubMed

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