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Coeli M. Lopes, Ph.D.

Contact Information

Phone Numbers

Administrative: (585) 276-7698

Office: (585) 276-7692

Fax: (585) 276-9829

Research Labs

The major focus of Dr. Lopes current work involves the regulation of the slow delayed rectifier-like current (IKs) in the heart and the pathogenesis of the Long QT (LQT1) syndrome.

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Faculty Appointments


Sudden arrhythmic death is the major cause of death in patients with congestive heart failure. In addition, heart failure increases the proarrhythmic effect of antiarrhythmic drugs, with the risk of drug induced Torsades de Pointes arrhythmias being approximately doubled by heart failure. Nonetheless the mechanisms of regulation of ion channels in heart failure are incompletely understood. Our works aims to undertand the pathological remodeling of cardiac ion currents in heart failure in order to develop novel treatements to reverse these effects and treat life treatening arrhythmias. We also study the effect of genetic mutations linked to the inherited cardiac arrhythmia Long QT syndrome. We try to understand the role of specific genetic mutations on the patient clinical phenotype and response to treatment. Identification of disease- and mutation- specific therapies will ultimately allow tailoring of therapy to patients, optimizing treatment and lowering the overall risk of life threatening cardiac arrhythmias.

Professional Background


BS: PUC-Rio, Brazil; Physics (1989)
MS: PUC-Rio, Brazil; Biophysics (1992)
PhD: Imperial College, UK; Biophysics (1997)
Postdoctoral Fellow - Yale University - Department of Physiology (1997-2000)
Postdoctoral Fellow - Mount Sinai School of Medicine - Department of Physiology and Biophysics (2000-2003)

2003-2004: Instructor - Mount Sinai School of Medicine - Department of Physiology and Biophysics
2004-2012: Assistant Professor - University of Rochester - Department of medicine - Cardiovascular Research Institute
2013-now: Associate Professor (Research) - University of Rochester - Department of medicine - Cardiovascular Research Institute


We are interested in understanding the regulation of ion channels by diverse G-protein signaling pathways in normal and pathological states.

One major focus of our current work involves the changes in function and regulation of cardiac ion channels that lead to the pathogenesis of the Long QTsyndrome. Our work attempts to translate channel function and dysregulation at the cellular level to patient clinical phenotype and response to treatment.

A second focus of our current research is the study of the pathological remodeling of the slow delayed rectifier-like current (IKs) in heart failure. KCNQ1 is co-assembled with the KCNE1 gene product in the heart to produce IKs, which is one of the main currents responsible for myocyte repolarization. The most commonly inherited cardiac arrhythmia, long-QT1 (LQT1), is due to mutations in the KCNQ1 potassium channel. Heart disease is also known to decrease IKs currents. Our current research focus on stress signals caused by chronic stimulation of kinase signaling pathways, and their consequence for ion channel function and membrane trafficking. We explore possible novel antiarrhythmic treatments to reverse IKs pathological remodeling during heart failure.



BS | Brazil-Pontificia Universidade Catolica

MS | Brazil-Pontificia Universidade Catolica

PhD | Imperial College


NIH reviewer ESTA Study Section

2012 - Present
AHA reviewer - Cardiac Electrophysiology Study Section

2004 - Present
Scientist Development Grant
Sponsor: American Heart Association

2002 - 2004
Postdoctoral Fellowship American Heart Association

New York City Board Fellow Award American Heart Association

1992 - 1996
PhD Scholarship Federal Agency for Post-Graduate Education (CAPES- Brazil)

1990 - 1992
Graduate Student Scholarship National Research Council (CNPq Brazil)

Outstanding Basic Science Student Award PUC-Rio

1986 - 1989
Full Merit University Scholarship PUC-Rio

Outstanding Basic Science Student Award PUC-Rio

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Journal Articles

Roberts JD, Krahn AD, Ackerman MJ, Rohatgi RK, Moss AJ, Nazer B, Tadros R, Gerull B, Sanatani S, Wijeyeratne YD, Baruteau AE, Muir AR, Pang B, Cadrin-Tourigny J, Talajic M, Rivard L, Tester DJ, Liu T, Whitman IR, Wojciak J, Conacher S, Gula LJ, Leong-Sit P, Manlucu J, Green MS, Hamilton R, Healey JS, Lopes CM, Behr ER, Wilde AA, Gollob MH, Scheinman MM. "Loss-of-Function Variants: True Monogenic Culprits of Long-QT Syndrome or Proarrhythmic Variants Requiring Secondary Provocation?" Circulation. Arrhythmia and electrophysiology.. 2017 Aug 0; 10(8)

Ruwald MH, Parks XX, Moss AJ, Zareba W, Baman J, McNitt S, Kanters JK, Shimizu W, Wilde AA, Jons C, Lopes CM. "Stop-codon and C-terminal nonsense mutations are associated with a lower risk of cardiac events in patients with long QT syndrome type 1." Heart rhythm.. 2016 Jan 0; 13(1):122-31. Epub 2015 Aug 28.

O-Uchi J, Sorenson J, Jhun BS, Mishra J, Hurst S, Williams K, Sheu SS, Lopes CM. "Isoform-specific dynamic translocation of PKC by ?1-adrenoceptor stimulation in live cells." Biochemical and biophysical research communications.. 2015 Sep 25; 465(3):464-70. Epub 2015 Aug 12.

Books & Chapters

Chapter Title: Single cell electrophysiology and ion channelopathies
Book Title: The molecular genetics of cardiac electrophysiology
Author List: C.M. Lopes, Goldstein S.A., Apkon M.
Edited By: CI Berul, J Tobin
Published By: Kluwer Academic Publishers 2000




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