Natalia Shirokova

ORCID: 0000-0003-4648-4592
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About
Contact & Profiles
Research Areas
  • Ion channel regulation and function
  • Muscle Physiology and Disorders
  • Neuroscience and Neural Engineering
  • Cardiac electrophysiology and arrhythmias
  • Cardiomyopathy and Myosin Studies
  • Mitochondrial Function and Pathology
  • Cardiovascular Effects of Exercise
  • Genetic Neurodegenerative Diseases
  • Connexins and lens biology
  • Adipose Tissue and Metabolism
  • Neuroscience and Neuropharmacology Research
  • Atrial Fibrillation Management and Outcomes
  • Cardiac Arrhythmias and Treatments
  • Ion Channels and Receptors
  • Muscle activation and electromyography studies
  • Cardiac Ischemia and Reperfusion
  • Neurological disorders and treatments
  • Redox biology and oxidative stress
  • Cardiovascular Function and Risk Factors
  • Neurobiology and Insect Physiology Research
  • Electrochemical sensors and biosensors
  • Piperaceae Chemical and Biological Studies
  • ATP Synthase and ATPases Research
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Autophagy in Disease and Therapy

Rutgers New Jersey Medical School
2006-2023

Rutgers, The State University of New Jersey
2012-2023

Rutgers Health
2018-2022

Research Centre for Medical Genetics
2019-2020

Columbia University
2013

Valley Health System
2013

State Research Center of the Russian Federation
2010-2012

University Hospital, Newark
2009-2012

Moscow Academy of Education Natalia Nesterova
2012

Rush University
1992-2001

Fluo‐3 fluorescence associated with Ca 2+ release was recorded confocal microscopy in single muscle fibres mechanically dissected from fast twitch of rats or frogs, voltage clamped a two Vaseline‐gap chamber. Interventions that elicited sparks frog skeletal (low depolarizations, application caffeine) generated rat images consistent substantial triadic regions, but devoid resolvable discrete events. were never observed adult fibres. In contrast, standard morphology abundant myotubes embryonic...

10.1111/j.1469-7793.1998.377be.x article EN The Journal of Physiology 1998-10-01

Puzzled by recent reports of differences in specific ligand binding to muscle Ca2+ channels, we quantitatively compared the flux release from sarcoplasmic reticulum (SR) skeletal fibers an amphibian (frog) and a mammal (rat), voltage clamped double Vaseline gap chamber. The determinations were carried out "removal" method measuring rate dyes large excess over other buffers. To have more meaningful comparison, effects stretching fibers, rapid changes temperature, content SR studied both...

10.1085/jgp.107.1.1 article EN The Journal of General Physiology 1996-01-01

Cardiac myopathies are the second leading cause of death in patients with Duchenne and Becker muscular dystrophy, two most common severe forms a disabling striated muscle disease. Although genetic defect has been identified as mutations dystrophin gene, very little is known about molecular cellular events to progressive cardiac damage. Dystrophin protein linking cytoskeleton complex transmembrane proteins that interact extracellular matrix. The fragility cell membrane resulting from lack...

10.1093/cvr/cvm089 article EN Cardiovascular Research 2007-12-04

AimsTo study the potential efficacy of ganglionated plexi (GP) ablation in setting longstanding persistent atrial fibrillation (AF).

10.1093/europace/euq014 article EN EP Europace 2010-02-20

Aberrant expression of the cardiac gap junction protein connexin-43 (Cx43) has been suggested as playing a role in development disease mdx mouse model Duchenne muscular dystrophy (DMD); however, mechanistic understanding this association is lacking. Here, we identified reduction phosphorylation Cx43 serines S325/S328/S330 human and DMD hearts. We hypothesized that hypophosphorylation serine-triplet triggers pathological redistribution to lateral sides cardiomyocytes (remodeling). Therefore,...

10.1172/jci128190 article EN Journal of Clinical Investigation 2020-01-07

Patients with Duchenne muscular dystrophy (DMD) commonly present severe ventricular arrhythmias that contribute to heart failure. Arrhythmias and lethality are also consistently observed in adult Dmdmdx mice, a mouse model of DMD, after acute β-adrenergic stimulation. These pathological features were previously linked aberrant expression remodeling the cardiac gap junction protein connexin43 (Cx43). Here, we report remodeled Cx43 forms hemichannels lateral membrane cardiomyocytes agonist...

10.1172/jci.insight.130091 article EN JCI Insight 2019-11-21

In many types of muscle, intracellular Ca 2+ release for contraction consists brief sparks. Whether these result from the opening one or channels in sarcoplasmic reticulum is not known. Examining massive numbers sparks frog skeletal muscle and evaluating their current, we provide evidence that they are generated by multiple channels. A mode demonstrated distribution spark rise times presence channel activator caffeine. This finding contradicts expectations single evolving reversibly, but a...

10.1073/pnas.070056497 article EN Proceedings of the National Academy of Sciences 2000-04-04

The role of mitochondrial Ca2+ transport in regulating intracellular signaling and enzymes involved energy metabolism is widely recognized many tissues. However, the ability skeletal muscle mitochondria to sequester released from sarcoplasmic reticulum (SR) during contraction-relaxation cycle still disputed. To assess functional cross-talk between SR mitochondria, we examined mutual relationship connecting cytosolic dynamics permeabilized fibers. Cytosolic transients were recorded with...

10.1074/jbc.m505024200 article EN cc-by Journal of Biological Chemistry 2005-10-11

Abstract Aims Duchenne muscular dystrophy (DMD) is an inherited devastating muscle disease with severe and often lethal cardiac complications. Emerging evidence suggests that the evolution of pathology in DMD accompanied by accumulation mitochondria defective structure function. Here, we investigate whether defects housekeeping autophagic pathway contribute to mitochondrial metabolic dysfunctions dystrophic cardiomyopathy. Methods results We employed various biochemical imaging techniques...

10.1093/cvr/cvx201 article EN Cardiovascular Research 2017-10-04

Intact skeletal muscle fibres from adult mammals exhibit neither spontaneous nor stimulated Ca(2+) sparks. Mechanical or chemical skinning procedures have been reported to unmask The present study investigates the mechanisms that determine development of spark activity in permeabilized dissected muscles with different metabolic capacity. Spontaneous sparks were detected fluo-3 and single photon confocal microscopy; mitochondrial redox potential was evaluated NADH signals recorded two-photon...

10.1113/jphysiol.2005.086280 article EN The Journal of Physiology 2005-04-22

Ca 2+ sparks, localized elevations in cytosolic [Ca ], are rarely detected intact adult mammalian skeletal muscle under physiological conditions. However, they have been observed permeabilized cells and fibres subjected to stresses, such as osmotic shock strenuous exercise. Our previous studies indicated that an excess cellular reactive oxygen species (ROS) generation over the ROS scavenging capabilities could be one of up‐stream causes spark appearance fibres. Here we tested whether balance...

10.1113/jphysiol.2007.146571 article EN The Journal of Physiology 2007-11-02

Duchenne muscular dystrophy (DMD) is a muscle disease with serious cardiac complications. Changes in Ca2+ homeostasis and oxidative stress were recently associated deterioration, but the cellular pathophysiological mechanisms remain elusive. We investigated whether activity of ryanodine receptor (RyR) release channels affected, changes function are cause or consequence which post-translational modifications drive progression. Electrophysiological, imaging, biochemical techniques used to...

10.1093/cvr/cvs425 article EN Cardiovascular Research 2012-12-21

AimsNicotinamide adenine dinucleotide oxidases (NOXs) are important contributors to cellular oxidative stress in the cardiovascular system. The NOX2 isoform is upregulated numerous disorders, including dystrophic cardiomyopathy, where it drives progression of disease. However, mechanisms underlying overexpression still unknown. We investigated role microRNAs (miRs) regulation expression.

10.1093/cvr/cvv238 article EN public-domain Cardiovascular Research 2015-10-26

Connexin-43 (Cx43) is the most abundant protein forming gap junction channels (GJCs) in cardiac ventricles. In multiple pathologies, including hypertrophy and heart failure, Cx43 found remodeled at lateral side of intercalated discs ventricular cardiomyocytes. Remodeling has been long linked to spontaneous arrhythmia, yet mechanisms by which arrhythmias develop are still debated. Using a model dystrophic cardiomyopathy, we previously showed that function as aberrant hemichannels (non-forming...

10.1085/jgp.202213150 article EN cc-by-nc-sa The Journal of General Physiology 2023-05-16

Fluo‐3 fluorescence associated with Ca 2+ release was recorded confocal microscopy in single muscle fibres. Clamp depolarization to −65 or −60 mV elicited sparks amplitudes and spatial widths distributed approximately normally, mean values of 0.79 resting 0.8 μm ( S.D. , 0.17 0.2 μm; n = 193 ), respectively. Given these distributions, events amplitude less than 0.45 width 0.4 are unlikely be sparks. Low voltage (−72 mV) only one spark per triad every 6 s, but generated a relative increase at...

10.1111/j.1469-7793.1997.003bl.x article EN The Journal of Physiology 1997-07-01

An algorithm for the calculation of Ca2+ release flux underlying sparks (Blatter, L.A., J. Hüser, and E. Ríos. 1997. Proc. Natl. Acad. Sci. USA. 94:4176–4181) was modified applied to obtained by confocal microscopy in single frog skeletal muscle fibers, which were voltage clamped a two-Vaseline gap chamber or permeabilized immersed fluo-3–containing internal solution. The performance characterized on simulation fluorescence due from spherical source, homogeneous three-dimensional space that...

10.1085/jgp.114.1.31 article EN The Journal of General Physiology 1999-07-01

Amplitude, spatial width, and rise time of Ca2+ sparks were compared in frog fast-twitch muscle, three conditions that alter activation release channels by [Ca2+]. A total ∼17,000 from 30 cells evaluated. In under voltage clamp, caffeine (0.5 or 1 mM) increased average spark width 28%, 18%, amplitude 7%. Increases significant even among events the same time. Spontaneous recorded permeabilized fibers with low internal [Mg2+] (0.4 mM), had times greater than reference, not significantly...

10.1085/jgp.115.2.139 article EN The Journal of General Physiology 2000-02-01
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