Overview

1987-1990: Aspirant MPhTI in the Bogomoletz Institute of Physiology, Kiyv, Ukraine (Advisors: Drs. P.Kostyuk, I. Magura).
1990-1997: Research Associate of the Department of General Physiology of the Nervous System, Bogomoletz Institute
of Physiology, Kyiv, Ukraine.
1991-1996: Research Associate in the Department Molecular Biophysics and Physiology, Rush University, Chicago, IL,
USA (Advisor: Dr. E, Rios).
1996-2000: Assistant Professor (non-tenure track) in the Department Molecular Biophysics and Physiology, Rush
University, Chicago, IL, USA.
2000-2009: Assistant Professor (tenure track) in the Department of Pharmacology and Physiology, UMDNJ-New Jersey
Medical School, Newark, NJ, USA.
2009-date: Associate Professor with tenure in the Department of Pharmacology, Physiology, Neuroscience, UMDNJ and
later NJMS, Rutgers, Newark, NJ, USA.

Education

PHD, 1991, Bogomoletz Institute of Physiology
M.S., 1987, Moscow Institute of Physics & Technology, Russia
B.S., 1984, Moscow Institute of Physics & Technology, Russia

Curriculum Vitae

View CV

Relevant Publications

C. Kang, M.A. Badr, V. Kyrychenko, E.-L. Eskelinen, and N. Shirokova. Deficit in PINK1/PARKIN-mediated mitochondrial autophagy at late stages of dystrophic cardiomyopathy. (2018). Cardiovascular Research 114:90-102.

J.P. Gonzalez, J. Ramachandran, E. Himelman, M.A. Badr, C. Kang, J. Nuet, N. Fefelova, L.-H. Xie, N. Shirokova*, J.E. Contreras* and D. Fraidenraich*. Normalization of connexin 43 protein levels prevents cellular and functional signs of dystrophic cardiomyophaty in mice. (2018). Journal of Neuromuscular Disorders 28:361-372. *Corresponding authors.

S. Kyrychenko, V. Kyrychenko, M.A. Badr, Y. Ikeda, J. Sadoshima and N. Shirokova. Pivotal role of miRNA-448 in the development of ROS-derived dystrophic cardiomyopathy. (2015). Cardiovascular Research 108:324-334.

V. Kyrychenko, E. Polakova, R. Yanichek and N. Shirokova. Mitochondrial dysfuctions during progression of dystrophic cardiomyopathy. (2015). Cell Calcium 58:186-195.

S. Kyrychenko, E. Polakova, C. Kang, K. Pocsai, N.D. Ullrich, E. Niggli and N. Shirokova.. Hierarchical accumulations of Ryr posttranslational modifications drive disease progression in dystrophic cardiomyopathy. (2013) Cardiovascular Research, 97:666-675.

N. Shirokova and E. Niggli. Cardiac Phenotype of Duchenne Muscular Dystrophy: Insights from Cellular Studies. (2013). Journal of Molecular and Cellular Cardiology 58:217-224.

V.M. Shkryl, A.S. Martins, N.D. Ullrich, M.C. Nowycky, E. Niggli and N. Shirokova. (2009). Reciprocal amplification of ROS and Ca2+ signals in stressed mdx dystrophic skeletal muscle fibers. Pflugers Archive 458: 915-928.

W.J. Durham, P. Aracena-Parks, C. Long, A.E. Rossi, S.A. Goonasekera, S. Boncompagni, D.L. Galvan, C.P. Gilman, M. Baker, N. Shirokova, F. Protasi, R. Dirksen and S.L. Hamilton. (2008). RyR1 S-Nitrosylation underlies environmental heat stroke and sudden death in Y522S RyR1 knock-in mice. Cell, 133: 53-65.

C. Jung, A.S. Martins, E. Niggli and N. Shirokova. Dystrophic cardiomyopathy: amplification of cellular damage by Ca2+ signalling and reactive oxygen species-generating pathways. (2008). Cardiovascular Research, 77: 766-773.

A.S. Martins, V.M. Shkryl, M.C. Nowycky and N. Shirokova. Reactive oxygen species contribute to Ca2+ signals produced by osmotic stress in mouse skeletal muscle fibres. (2008). Journal of Physiology, 586: 197-210.

Areas Of Interest

"mitophagy"

"Cx43"

"NOX2"

"PINK/PARKIN"

"RyR"

"calcium signaling"

"micro-RNA"

"mitochondria"

"muscular dystrophy"

"redox signaling"

Course List

CBNP5036Q		Mol Phys of Cell Comm
DENT5065Q		Dental Physiology
EDUC6101K		MSK & Integumentary Systems
EDUC6102K		Cardiovascular System

Cellular Mechanisms of Cardiac Dystrophy.

Duchenne muscular dystrophy (DMD) represents a severe inherited disease of striated muscle. It is caused by a mutation
of the dystrophin gene and characterized by a progressive loss of muscle function. Most DMD patients develop a
cardiomyopathy resulting in dilated hypertrophy and heart failure. The cellular and molecular mechanisms underlying the
development of cardiac dystrophy are investigated in this project. In particular we are looking at how NOX-2 driven
oxidative stress, augmented calcium signaling, mitochondrial pathology/impaired mitophagy as well as remodeling of
connexins contribute to cellular pathology of the disease. In our work, we utilize cellular electrophysiology, photometry,
confocal imaging, multiple biochemical and molecular biology techniques, as well as assessment of cardiac functions with
EKG and Echo.