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

Kód výsledku v 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>

Výsledek na webu

<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>

Jazyk výsledku

angličtina

Název v původním jazyce

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

Popis výsledku v původním jazyce

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.

Název v anglickém jazyce

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

Popis výsledku anglicky

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.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30105 - Physiology (including cytology)

Projekt

<a href="/cs/project/NV15-27735A" target="_blank" >NV15-27735A: Rozvoj chronického srdečního selhání a kardiorenálního syndromu u hypertenzních potkanů po infarktu myokardu: úloha epoxyeikosatrienových kyselin.</a><br>

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2017

Kód důvěrnosti údajů

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

Název periodika

Canadian Journal of Physiology and Pharmacology

ISSN

0008-4212

e-ISSN

—

Svazek periodika

95

Číslo periodika v rámci svazku

10

Stát vydavatele periodika

CA - Kanada

Počet stran výsledku

7

Strana od-do

1163-1169

Kód UT WoS článku

000411898100011

EID výsledku v databázi Scopus

2-s2.0-85030100296