Evidence of necroptosis in hearts subjected to various forms of ischemic insults

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F17%3A00479705" target="_blank" >RIV/67985823:_____/17:00479705 - isvavai.cz</a>

Result on the web

<a href="http://dx.doi.org/10.1139/cjpp-2016-0609" target="_blank" >http://dx.doi.org/10.1139/cjpp-2016-0609</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1139/cjpp-2016-0609" target="_blank" >10.1139/cjpp-2016-0609</a>

Result language

angličtina

Original language name

Evidence of necroptosis in hearts subjected to various forms of ischemic insults

Original language description

Long-lasting ischemia can result in cell loss, however, repeated episodes of brief ischemia increase the resistance of the heart against deleterious effects of subsequent prolonged ischemic insult and promote cell survival. Traditionally, it is believed that the supply of blood to the ischemic heart is associated with release of cytokines, activation of inflammatory response, and induction of necrotic cell death. In the past few years, this paradigm of passive necrosis as an uncontrolled cell death has been re-examined and the existence of a strictly regulated form of necrotic cell death, necroptosis, has been documented. This controlled cell death modality, resembling all morphological features of necrosis, has been investigated in different types of ischemia-associated heart injuries. The process of necroptosis has been found to be dependent on the activation of RIP1-RIP3-MLKL axis, which induces changes leading to the rupture of cell membrane. This pathway is activated by TNF-alpha, which has also been implicated in the cardioprotective signaling pathway of ischemic preconditioning. Thus, this review is intended to describe the TNF-alpha-mediated signaling leading to either cell survival or necroptotic cell death. In addition, some experimental data suggesting a link between heart dysfunction and the cellular loss due to necroptosis are discussed in various conditions of myocardial ischemia.

Czech name

—

Czech description

—

Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

—

OECD FORD branch

30105 - Physiology (including cytology)

Project

<a href="/en/project/NV15-27735A" target="_blank" >NV15-27735A: Progression of chronic heart failure and cardiorenal syndrome in hypertensive rats after myocardial infarction: role of epoxyeicosatrienoic acids.</a><br>

Continuities

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year

2017

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

Canadian Journal of Physiology and Pharmacology

ISSN

0008-4212

e-ISSN

—

Volume of the periodical

95

Issue of the periodical within the volume

10

Country of publishing house

CA - CANADA

Number of pages

7

Pages from-to

1163-1169

UT code for WoS article

000411898100011

EID of the result in the Scopus database

2-s2.0-85030100296