Anna Malashicheva

Dr. Anna Malashicheva

Institute of Cytology, Saint Petersburg, Sankt-Peterburg, Russia
orcid

Research Focus & Metrics

Academic Career Length

29Years (1998-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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22 September 2017 in Journal of the American Heart Association
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Journal Article
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ARArkady Rutkovskiy
Arkady Rutkovskiy
Anna MalashichevaAnna Malashicheva
Anna Malashicheva
Gareth SullivanGareth Sullivan
Gareth Sullivan
MBMaria Bogdanova
Maria Bogdanova
AKAnna Kostareva
Anna Kostareva
JVJarle Vaage
Jarle Vaage
Aortic valve stenosis due to calcification of the valve leaflets is the most common valve disease in the developed world. It is the third leading cause of cardiovascular disease.[1][1] Risk factors include male gender, smoking, diabetes mellitus, hypertension, high levels of circulating lipids, and

1 January 2013 in Stem Cell Research
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DCDiana Coronado
Diana Coronado
MGMurielle Godet
Murielle Godet
PBPierre-Yves Bourillot
Pierre-Yves Bourillot
YTYann Tapponnier
Yann Tapponnier
ABAgnieszka Bernat
Agnieszka Bernat
PSPierre Savatier
Pierre Savatier
A short G1 phase is a characteristic feature of mouse embryonic stem cells (ESCs). To determine if there is a causal relationship between G1 phase restriction and pluripotency, we made use of the Fluorescence Ubiquitination Cell Cycle Indicator (FUCCI) reporter system to FACS-sort ESCs in the different cell cycle phases. Hence, the G1 phase cells appeared to be more susceptible to differentiation, particularly when ESCs self-renewed in the naïve state of pluripotency. Transitions from ground to naïve, then from naïve to primed states of pluripotency were associated with increased durations of the G1 phase, and cyclin E-mediated alteration of the G1/S transition altered the balance between self-renewal and differentiation. LIF withdrawal resulted in a lengthening of the G1 phase in naïve ESCs, which occurred prior to the appearance of early lineage-specific markers, and could be reversed upon LIF supplementation. We concluded that the short G1 phase observed in murine ESCs was a determinant of naïve pluripotency and was partially under the control of LIF signaling.

10 December 2020 in Science
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CTChristina V. Theodoris
Christina V. Theodoris
PZPing Zhou
Ping Zhou
LLLei Liu
Lei Liu
Yu ZhangYu Zhang
Yu Zhang
TNTomohiro Nishino
Tomohiro Nishino
DSDeepak Srivastava
Deepak Srivastava
Machine learning for medicine: Small-molecule screens aimed at identifying therapeutic candidates traditionally search for molecules that affect one to several outputs at most, limiting discovery of true disease-modifying drugs. Theodoris et al. developed a machine-learning approach to identify small molecules that broadly correct gene networks dysregulated in a human induced pluripotent stem cell disease model of a common form of heart disease involving the aortic valve. Gene network correction by the most efficacious therapeutic candidate generalized to primary aortic valve cells derived from more than 20 patients with sporadic aortic valve disease and prevented aortic valve disease in vivo in a mouse model. Science , this issue p. eabd0724

23 April 2020 in Nanomaterials
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DSDmitry Leonidovich Sonin
Dmitry Leonidovich Sonin
EPEvgeniia Pochkaeva
Evgeniia Pochkaeva
SZSergei Zhuravskii
Sergei Zhuravskii
VPViktor Postnov
Viktor Postnov
DKDmitry Korolev
Dmitry Korolev
MGMichael Galagudza
Michael Galagudza
The effect of unmodified chitosan nanoparticles with a size of ~100 nm and a weakly positive charge on blood coagulation, metabolic activity of cultured cardiomyocytes, general toxicity, biodistribution, and reactive changes in rat organs in response to their single intravenous administration at doses of 1, 2, and 4 mg/kg was studied. Chitosan nanoparticles (CNPs) have a small cytotoxic effect and have a weak antiplatelet and anticoagulant effect. Intravenous administration of CNPs does not cause significant hemodynamic changes, and 30 min after the CNPs administration, they mainly accumulate in the liver and lungs, without causing hemolysis and leukocytosis. The toxicity of chitosan nanoparticles was manifested in a dose-dependent short-term delay in weight gain with subsequent recovery, while in the 2-week observation period no signs of pain and distress were observed in rats. Granulomas found in the lungs and liver indicate slow biodegradation of chitosan nanoparticles. In general, the obtained results indicate a good tolerance of intravenous administration of an unmodified chitosan suspension in the studied dose range.

1 April 2016 in Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
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Journal Article
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AKAleksandra S. Kostina
Aleksandra S. Kostina
VUVladimir Е. Uspensky
Vladimir Е. Uspensky
OIOlga Irtyuga
Olga Irtyuga
EIElena V. Ignatieva
Elena V. Ignatieva
OFOlga Freylikhman
Olga Freylikhman
Anna MalashichevaAnna Malashicheva
Anna Malashicheva

Verified
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OKOlga Kachanova
Olga Kachanova
ALArseniy Lobov
Arseniy Lobov
Anna MalashichevaAnna Malashicheva
Anna Malashicheva
Myocardial infarction (MI) is a pathological process, evidencing as massive death of cardiomyocytes associated with hypoxic and oxidative stress. The formation of areas of fibrosis ultimately leads to heart failure. There are some mechanisms that contribute to the functional repair of the heart. In most mammals, including humans, the Notch signaling pathway has cardioprotective effects. It is involved in the formation of the heart in embryogenesis and in the restoration of cardiac function after MI due to: (1) reducing oxidative stress; (2) prevention of apoptosis; (3) regulation of inflammation; (4) containment of fibrosis and hypertrophy of cardiomyocytes; (5) tissue revascularization; and (6) regulation of proliferation and differentiation of cardiomyocytes. In addition, the Notch signaling pathway interacts with other signaling cascades involved in the pathogenesis of MI and subsequent cardiac repair. In this review, we consider the Notch signaling pathway as a potential target for therapeutic approaches aimed at improving cardiac recovery after MI.