Atrazine increases hepatic inflammation and injury via endoplasmic reticulum (ER) stress mediated excessive formation of mitochondria-associated membranes (MAMs) and activation of the cGAS-STING pathw
6 hours ago
- #ER Stress
- #Atrazine
- #Liver Injury
- Atrazine (ATR) exposure induces hepatic inflammation and injury through a specific mechanistic pathway.
- The pathway involves endoplasmic reticulum (ER) stress leading to excessive formation of mitochondria-associated membranes (MAMs).
- This results in mitochondrial calcium overload, increased mitochondrial reactive oxygen species (mtROS), and cytosolic release of mitochondrial DNA (mtDNA).
- Cytosolic mtDNA activates the cGAS-STING pathway and NLRP3 inflammasome, triggering a severe hepatic inflammatory response.
- Inhibition of ER stress with 4-PBA reduces MAMs over-assembly and mitigates mitochondrial dysfunction.
- Scavenging mitochondrial ROS with MitoQ attenuates downstream inflammatory activation.
- The study provides new insights into ATR-induced hepatotoxicity and suggests potential therapeutic strategies for pollutant-induced liver injury.