Regulation of cell death by mitochondrial transport systems of calcium and BCL‐2 proteins

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61388955%3A_____%2F20%3A00533843" target="_blank" >RIV/61388955:_____/20:00533843 - isvavai.cz</a>

Výsledek na webu

<a href="http://hdl.handle.net/11104/0312095" target="_blank" >http://hdl.handle.net/11104/0312095</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.3390/membranes10100299" target="_blank" >10.3390/membranes10100299</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Regulation of cell death by mitochondrial transport systems of calcium and BCL‐2 proteins

Popis výsledku v původním jazyce

Mitochondria represent the fundamental system for cellular energy metabolism, by not only supplying energy in the form of ATP, but also by affecting physiology and cell death via the regulation of calcium homeostasis and the activity of Bcl‐2 proteins. A lot of research has recently been devoted to understanding the interplay between Bcl‐2 proteins, the regulation of these interactions within the cell, and how these interactions lead to the changes in calcium homeostasis. However, the role of Bcl‐2 proteins in the mediation of mitochondrial calcium homeostasis, and therefore the induction of cell death pathways, remain underestimated and are still not well understood. In this review, we first summarize our knowledge about calcium transport systems in mitochondria, which, when miss‐regulated, can induce necrosis. We continue by reviewing and analyzing the functions of Bcl‐2 proteins in apoptosis. Finally, we link these two regulatory mechanisms together, exploring the interactions between the mitochondrial Ca2+ transport systems and Bcl‐2 proteins, both capable of inducing cell death, with the potential to determine the cell death pathway—either the apoptotic or the necrotic one.

Název v anglickém jazyce

Regulation of cell death by mitochondrial transport systems of calcium and BCL‐2 proteins

Popis výsledku anglicky

Mitochondria represent the fundamental system for cellular energy metabolism, by not only supplying energy in the form of ATP, but also by affecting physiology and cell death via the regulation of calcium homeostasis and the activity of Bcl‐2 proteins. A lot of research has recently been devoted to understanding the interplay between Bcl‐2 proteins, the regulation of these interactions within the cell, and how these interactions lead to the changes in calcium homeostasis. However, the role of Bcl‐2 proteins in the mediation of mitochondrial calcium homeostasis, and therefore the induction of cell death pathways, remain underestimated and are still not well understood. In this review, we first summarize our knowledge about calcium transport systems in mitochondria, which, when miss‐regulated, can induce necrosis. We continue by reviewing and analyzing the functions of Bcl‐2 proteins in apoptosis. Finally, we link these two regulatory mechanisms together, exploring the interactions between the mitochondrial Ca2+ transport systems and Bcl‐2 proteins, both capable of inducing cell death, with the potential to determine the cell death pathway—either the apoptotic or the necrotic one.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10403 - Physical chemistry

Projekt

<a href="/cs/project/GA18-04871S" target="_blank" >GA18-04871S: Oxidační stres jako důležitý modulátor apoptotické aktivity Baxu: molekulární pohled pomocí fluorescence jednotlivých molekul</a><br>

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2020

Kód důvěrnosti údajů

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

Název periodika

Membranes

ISSN

2077-0375

e-ISSN

—

Svazek periodika

10

Číslo periodika v rámci svazku

10

Stát vydavatele periodika

CH - Švýcarská konfederace

Počet stran výsledku

32

Strana od-do

299

Kód UT WoS článku

000586146500001

EID výsledku v databázi Scopus

2-s2.0-85093943795