Display options
Cite
Yamaguchi N, Xiao J, Narke D, et al. Cardiac Pressure Overload Decreases ETV1 Expression in the Left Atrium, Contributing to Atrial Electrical and Structural Remodeling. Circulation. 2020;143(8):805-820doi: 10.1161/CIRCULATIONAHA.120.048121.
Yamaguchi, N., Xiao, J., Narke, D., Shaheen, D., Lin, X., Offerman, E., Khodadadi-Jamayran, A., Shekhar, A., Choy, A., Wass, S. Y., Van Wagoner, D. R., Chung, M. K., & Park, D. S. (2021). Cardiac Pressure Overload Decreases ETV1 Expression in the Left Atrium, Contributing to Atrial Electrical and Structural Remodeling. Circulation, 143(8), 805-820. https://doi.org/10.1161/CIRCULATIONAHA.120.048121
Yamaguchi, Naoko, et al. "Cardiac Pressure Overload Decreases ETV1 Expression in the Left Atrium, Contributing to Atrial Electrical and Structural Remodeling." Circulation vol. 143,8 (2021): 805-820. doi: https://doi.org/10.1161/CIRCULATIONAHA.120.048121
Yamaguchi N, Xiao J, Narke D, Shaheen D, Lin X, Offerman E, Khodadadi-Jamayran A, Shekhar A, Choy A, Wass SY, Van Wagoner DR, Chung MK, Park DS. Cardiac Pressure Overload Decreases ETV1 Expression in the Left Atrium, Contributing to Atrial Electrical and Structural Remodeling. Circulation. 2021 Feb 23;143(8):805-820. doi: 10.1161/CIRCULATIONAHA.120.048121. Epub 2020 Nov 23. PMID: 33225722; PMCID: PMC8449308.
Copy Download .nbib Format: NLM
Share it on

Circulation. 2021 Feb 23;143(8):805-820. doi: 10.1161/CIRCULATIONAHA.120.048121. Epub 2020 Nov 23.

Cardiac Pressure Overload Decreases ETV1 Expression in the Left Atrium, Contributing to Atrial Electrical and Structural Remodeling.

Circulation

Naoko Yamaguchi, Junhua Xiao, Deven Narke, Devin Shaheen, Xianming Lin, Erik Offerman, Alireza Khodadadi-Jamayran, Akshay Shekhar, Alex Choy, Sojin Y Wass, David R Van Wagoner, Mina K Chung, David S Park

Affiliations

  1. The Leon H. Charney Division of Cardiology (N.Y., J.X., D.N., D.S., X.L., E.O., A.S., D.S.P.), New York University Grossman School of Medicine.
  2. NYU Applied Bioinformatics Labs (A.K.-J.), New York University Grossman School of Medicine.
  3. Regeneron Pharmaceuticals Inc, Biotechnology, Tarrytown, NY (A.S.).
  4. Icahn Medical Institute at Mount Sinai, New York (A.C.).
  5. Department of Cardiovascular & Metabolic Sciences, Department of Cardiovascular Medicine, Cleveland Clinic, OH (S.Y.W., D.R.V.W., M.K.C.).

PMID: 33225722 PMCID: PMC8449308 DOI: 10.1161/CIRCULATIONAHA.120.048121

Abstract

BACKGROUND: Elevated intracardiac pressure attributable to heart failure induces electrical and structural remodeling in the left atrium (LA) that begets atrial myopathy and arrhythmias. The underlying molecular pathways that drive atrial remodeling during cardiac pressure overload are poorly defined. The purpose of this study is to characterize the response of the ETV1 (ETS translocation variant 1) signaling axis in the LA during cardiac pressure overload in humans and mouse models and explore the role of ETV1 in atrial electrical and structural remodeling.

METHODS: We performed gene expression profiling in 265 left atrial samples from patients who underwent cardiac surgery. Comparative gene expression profiling was performed between 2 murine models of cardiac pressure overload, transverse aortic constriction banding and angiotensin II infusion, and a genetic model of

RESULTS: Using the Cleveland Clinic biobank of human LA specimens, we found that

CONCLUSIONS: ETV1 is downregulated in the LA during cardiac pressure overload, contributing to both electrical and structural remodeling.

Keywords: atrial fibrillation; atrial remodeling; heart failure; signal transduction; transcription factors

References

  1. J Biol Chem. 2001 May 18;276(20):17058-62 - PubMed
  2. OMICS. 2012 May;16(5):284-7 - PubMed
  3. Circulation. 2009 Apr 14;119(14):1977-2016 - PubMed
  4. J Mol Cell Cardiol. 2011 Mar;50(3):522-33 - PubMed
  5. Nat Commun. 2016 Oct 04;7:12966 - PubMed
  6. Sci Rep. 2018 Jul 2;8(1):9944 - PubMed
  7. Nat Med. 2001 Nov;7(11):1236-40 - PubMed
  8. Circ Res. 2018 Aug 17;123(5):550-563 - PubMed
  9. Circ Genom Precis Med. 2018 Mar;11(3):e002107 - PubMed
  10. Bioinformatics. 2013 Jan 1;29(1):15-21 - PubMed
  11. Circ Res. 2020 Jan 17;126(2):182-196 - PubMed
  12. Circ Res. 1997 Dec;81(6):1045-52 - PubMed
  13. Bioinformatics. 2010 Mar 15;26(6):841-2 - PubMed
  14. J Clin Invest. 2000 Jun;105(11):1605-12 - PubMed
  15. Bioinformatics. 2015 Jan 15;31(2):166-9 - PubMed
  16. Heart Rhythm. 2016 Mar;13(3):762-70 - PubMed
  17. J Mol Cell Cardiol. 2014 Sep;74:330-9 - PubMed
  18. Curr Heart Fail Rep. 2014 Dec;11(4):404-15 - PubMed
  19. Nature. 2010 Oct 14;467(7317):849-53 - PubMed
  20. J Clin Invest. 2015 Jan;125(1):403-12 - PubMed
  21. J Clin Invest. 2016 Dec 1;126(12):4444-4459 - PubMed
  22. Front Physiol. 2018 Oct 04;9:1380 - PubMed
  23. Am J Physiol. 1998 Mar;274(3):H747-51 - PubMed
  24. Circ Res. 2020 Dec 4;127(12):1536-1548 - PubMed
  25. Genome Biol. 2014;15(12):550 - PubMed
  26. BMC Cardiovasc Disord. 2019 Feb 15;19(1):40 - PubMed
  27. Onco Targets Ther. 2019 May 09;12:3531-3544 - PubMed
  28. Am J Physiol. 1994 Aug;267(2 Pt 2):H742-50 - PubMed
  29. Heart Rhythm. 2013 Dec;10(12):1886-94 - PubMed
  30. Prog Biophys Mol Biol. 2008 Oct-Nov;98(2-3):208-18 - PubMed
  31. Exp Ther Med. 2017 May;13(5):2123-2128 - PubMed
  32. Transl Oncol. 2013 Aug 01;6(4):405-12 - PubMed
  33. Cardiovasc Pathol. 2017 Sep - Oct;30:27-37 - PubMed
  34. Cell. 2000 May 26;101(5):485-98 - PubMed
  35. Mol Endocrinol. 2007 Aug;21(8):1835-46 - PubMed
  36. J Vis Exp. 2010 Apr 21;(38): - PubMed
  37. J Mol Cell Cardiol. 2014 Nov;76:159-68 - PubMed

Publication Types

Grant support