Mycotoxins and cellular senescence: the impact of oxidative stress, hypoxia, and immunosuppression

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F62690094%3A18470%2F23%3A50019656" target="_blank" >RIV/62690094:18470/23:50019656 - isvavai.cz</a>

Výsledek na webu

<a href="https://link.springer.com/article/10.1007/s00204-022-03423-x?utm_source=getftr&utm_medium=getftr&utm_campaign=getftr_pilot" target="_blank" >https://link.springer.com/article/10.1007/s00204-022-03423-x?utm_source=getftr&utm_medium=getftr&utm_campaign=getftr_pilot</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1007/s00204-022-03423-x" target="_blank" >10.1007/s00204-022-03423-x</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Mycotoxins and cellular senescence: the impact of oxidative stress, hypoxia, and immunosuppression

Popis výsledku v původním jazyce

Mycotoxins induce oxidative stress, hypoxia, and cause immunosuppressive effects. Moreover, emerging evidence show that mycotoxins have a potential of inducing cellular senescence, which are involved in their immunomodulatory effects. Mycotoxins upregulate the expression of senescence markers γ-H2AX, senescence-associated β-galactosidase, p53, p16, and senescence-associated secretory phenotype (SASP) inflammatory factors. Moreover, mycotoxins cause senescence-associated cell cycle arrest by diminishing cyclin D1 and Cdk4 pathways, as well as increasing the expression of p53, p21, and CDK6. Mycotoxins may induce cellular senescence by activating reactive oxygen species (ROS)-induced oxidative stress. In addition, hypoxia acts as a double-edged sword on cell senescence; it could both act as the stress-induced senescence and also hinder the onset of cellular senescence. The SASP inflammatory factors have the ability to induce an immunosuppressive environment, while mycotoxins directly cause immunosuppression. Therefore, there is a potential relationship between mycotoxins and cellular senescence that synergistically cause immunosuppression. However, most of the current studies have involved the effect of mycotoxins on cell cycle arrest, but only limited in-depth research has been carried out to link the occurrence of this condition (cell cycle arrest) with cellular senescence. © 2022, The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.

Název v anglickém jazyce

Mycotoxins and cellular senescence: the impact of oxidative stress, hypoxia, and immunosuppression

Popis výsledku anglicky

Mycotoxins induce oxidative stress, hypoxia, and cause immunosuppressive effects. Moreover, emerging evidence show that mycotoxins have a potential of inducing cellular senescence, which are involved in their immunomodulatory effects. Mycotoxins upregulate the expression of senescence markers γ-H2AX, senescence-associated β-galactosidase, p53, p16, and senescence-associated secretory phenotype (SASP) inflammatory factors. Moreover, mycotoxins cause senescence-associated cell cycle arrest by diminishing cyclin D1 and Cdk4 pathways, as well as increasing the expression of p53, p21, and CDK6. Mycotoxins may induce cellular senescence by activating reactive oxygen species (ROS)-induced oxidative stress. In addition, hypoxia acts as a double-edged sword on cell senescence; it could both act as the stress-induced senescence and also hinder the onset of cellular senescence. The SASP inflammatory factors have the ability to induce an immunosuppressive environment, while mycotoxins directly cause immunosuppression. Therefore, there is a potential relationship between mycotoxins and cellular senescence that synergistically cause immunosuppression. However, most of the current studies have involved the effect of mycotoxins on cell cycle arrest, but only limited in-depth research has been carried out to link the occurrence of this condition (cell cycle arrest) with cellular senescence. © 2022, The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30108 - Toxicology

Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2023

Kód důvěrnosti údajů

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

Název periodika

Archives of toxicology

ISSN

0340-5761

e-ISSN

1432-0738

Svazek periodika

97

Číslo periodika v rámci svazku

2

Stát vydavatele periodika

DE - Spolková republika Německo

Počet stran výsledku

12

Strana od-do

393-404

Kód UT WoS článku

000888695100001

EID výsledku v databázi Scopus

2-s2.0-85142544475