Mycotoxins have a potential of inducing cell senescence: A new understanding of mycotoxin immunotoxicity
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00179906%3A_____%2F23%3A10469228" target="_blank" >RIV/00179906:_____/23:10469228 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/62690094:18470/23:50020484
Výsledek na webu
<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=nfsxr1g4oL" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=nfsxr1g4oL</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1016/j.etap.2023.104188" target="_blank" >10.1016/j.etap.2023.104188</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Mycotoxins have a potential of inducing cell senescence: A new understanding of mycotoxin immunotoxicity
Popis výsledku v původním jazyce
Mycotoxins result in immune dysfunction and cause immune diseases in animals and humans. However, the mechanisms of immunotoxicity involved in mycotoxins have not been fully explored, and emerging evidence suggests that these toxins may promote their immunotoxicity via cellular senescence. Mycotoxins induce cell senescence after DNA damage, and activate signaling via the NF-& kappa;B and JNK pathways to promote the secretion of senescence-associated secretory phenotype (SASP) cytokines including IL-6, IL-8, and TNF-& alpha;. DNA damage can also over-activate or cleave poly (ADP-ribose) polymerase-1 (PARP-1), increase the expression of cell cycle inhibitory proteins p21, and p53, and induce cell cycle arrest and then senescence. These senescent cells further down-regulate proliferation-related genes and overexpress inflammatory factors resulting in chronic inflammation and eventual immune exhaustion. Here we review the underlying mechanisms by which mycotoxins trigger cell senescence and the potential roles of SASP and PARP in these pathways. This work will help to further understand the mechanisms of immunotoxicity involved in mycotoxins.
Název v anglickém jazyce
Mycotoxins have a potential of inducing cell senescence: A new understanding of mycotoxin immunotoxicity
Popis výsledku anglicky
Mycotoxins result in immune dysfunction and cause immune diseases in animals and humans. However, the mechanisms of immunotoxicity involved in mycotoxins have not been fully explored, and emerging evidence suggests that these toxins may promote their immunotoxicity via cellular senescence. Mycotoxins induce cell senescence after DNA damage, and activate signaling via the NF-& kappa;B and JNK pathways to promote the secretion of senescence-associated secretory phenotype (SASP) cytokines including IL-6, IL-8, and TNF-& alpha;. DNA damage can also over-activate or cleave poly (ADP-ribose) polymerase-1 (PARP-1), increase the expression of cell cycle inhibitory proteins p21, and p53, and induce cell cycle arrest and then senescence. These senescent cells further down-regulate proliferation-related genes and overexpress inflammatory factors resulting in chronic inflammation and eventual immune exhaustion. Here we review the underlying mechanisms by which mycotoxins trigger cell senescence and the potential roles of SASP and PARP in these pathways. This work will help to further understand the mechanisms of immunotoxicity involved in mycotoxins.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
30104 - Pharmacology and pharmacy
Návaznosti výsledku
Projekt
—
Návaznosti
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2023
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Environmental Toxicology and Pharmacology
ISSN
1382-6689
e-ISSN
1872-7077
Svazek periodika
101
Číslo periodika v rámci svazku
Jun
Stát vydavatele periodika
NL - Nizozemsko
Počet stran výsledku
8
Strana od-do
104188
Kód UT WoS článku
001034549900001
EID výsledku v databázi Scopus
2-s2.0-85162135629