Elena M Tchevkina

Prof. Elena M Tchevkina

Blokhin National medical research center of oncology
orcid

Research Focus & Metrics

Academic Career Length

16Years (2011-Present)

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

Representative Publications

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23 January 2018 in Cell Death & Differentiation
Verified
Journal Article
Open access
Lorenzo GalluzziLorenzo Galluzzi
Lorenzo Galluzzi
IVIlio Vitale
Ilio Vitale
SAStuart A. Aaronson
Stuart A. Aaronson
JAJohn M. Abrams
John M. Abrams
DADieter Adam
Dieter Adam
Guido KroemerGuido Kroemer
Guido Kroemer
Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field.

1 July 2003 in Nature Reviews Molecular Cell Biology
Verified
Journal Article
Closed access
PDF file
SOSten Orrenius
Sten Orrenius
BZBoris Zhivotovsky
Boris Zhivotovsky
PNPierluigi Nicotera
Pierluigi Nicotera

10 October 2008 in Cell Death & Differentiation
Verified
Journal Article
Open access
PDF file
Guido KroemerGuido Kroemer
Guido Kroemer
LGL Galluzzi
L Galluzzi
PVPeter Vandenabeele
Peter Vandenabeele
JAJ Abrams
J Abrams
EAE S Alnemri
E S Alnemri
GMG Melino
G Melino
Different types of cell death are often defined by morphological criteria, without a clear reference to precise biochemical mechanisms. The Nomenclature Committee on Cell Death (NCCD) proposes unified criteria for the definition of cell death and of its different morphologies, while formulating several caveats against the misuse of words and concepts that slow down progress in the area of cell death research. Authors, reviewers and editors of scientific periodicals are invited to abandon expressions like ‘percentage apoptosis’ and to replace them with more accurate descriptions of the biochemical and cellular parameters that are actually measured. Moreover, at the present stage, it should be accepted that caspase-independent mechanisms can cooperate with (or substitute for) caspases in the execution of lethal signaling pathways and that ‘autophagic cell death’ is a type of cell death occurring together with (but not necessarily by) autophagic vacuolization. This study details the 2009 recommendations of the NCCD on the use of cell death-related terminology including ‘entosis’, ‘mitotic catastrophe’, ‘necrosis’, ‘necroptosis’ and ‘pyroptosis’.

15 July 2011 in Cell Death & Differentiation
Verified
Journal Article
Closed access
PDF file
LGL Galluzzi
L Galluzzi
IVIlio Vitale
Ilio Vitale
JAJ M Abrams
J M Abrams
EAE S Alnemri
E S Alnemri
EBE H Baehrecke
E H Baehrecke
Guido KroemerGuido Kroemer
Guido Kroemer

9 February 2007 in Apoptosis
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Journal Article
Open access
PDF file
MOMartin Ott
Martin Ott
VGVladimir Gogvadze
Vladimir Gogvadze
SOSten Orrenius
Sten Orrenius
BZBoris Zhivotovsky
Boris Zhivotovsky
In addition to the well-established role of the mitochondria in energy metabolism, regulation of cell death has recently emerged as a second major function of these organelles. This, in turn, seems to be intimately linked to their role as the major intracellular source of reactive oxygen species (ROS), which are mainly generated at Complex I and III of the respiratory chain. Excessive ROS production can lead to oxidation of macromolecules and has been implicated in mtDNA mutations, ageing, and cell death. Mitochondria-generated ROS play an important role in the release of cytochrome c and other pro-apoptotic proteins, which can trigger caspase activation and apoptosis. Cytochrome c release occurs by a two-step process that is initiated by the dissociation of the hemoprotein from its binding to cardiolipin, which anchors it to the inner mitochondrial membrane. Oxidation of cardiolipin reduces cytochrome c binding and results in an increased level of “free” cytochrome c in the intermembrane space. Conversely, mitochondrial antioxidant enzymes protect from apoptosis. Hence, there is accumulating evidence supporting a direct link between mitochondria, oxidative stress and cell death.

1 October 1995 in Neuron
Verified
Journal Article
Closed access
MAMaria Ankarcrona
Maria Ankarcrona
JDJeannette M. Dypbukt
Jeannette M. Dypbukt
EBEmanuela Bonfoco
Emanuela Bonfoco
BZBoris Zhivotovsky
Boris Zhivotovsky
SOSten Orrenius
Sten Orrenius
PNPierluigi Nicotera
Pierluigi Nicotera