UNDERSTANDING THE CROSSTALK BETWEEN ENDOPLASMIC RETICULUM STRESS AND OXIDATIVE STRESS IN DISEASES
Session
Pharmaceutical and Natural Sciences
Description
The endoplasmic reticulum (ER) is a vital organel with many critical cell functions. Various intracellular and environmental factors may disrupt its function and lead to the accumulation of unfolded or misfolded proteins that cause ER stress and activate the unfolded protein response (UPR). UPR leads to disruption of intracellular calcium and redox homeostasis and mitochondrial dysfunction. When the redox is unbalanced, the antioxidant mechanism is disrupted and leads to oxidative stress. ER stress mediates oxidative stress and increases reactive oxygen species (ROS) by affecting mitochondrial function, thus causing apoptosis in various metabolic diseases including cancer. In this talk, I will discuss how ER stress mediates oxidative stress in various metabolic diseases, including cancer, and the potential development of drugs that target these integrated signaling pathways.
Proceedings Editor
Edmond Hajrizi
ISBN
978-9951-550-95-6
Location
UBT Lipjan, Kosovo
Start Date
28-10-2023 8:00 AM
End Date
29-10-2023 6:00 PM
DOI
10.33107/ubt-ic.2023.117
Recommended Citation
Akıllılari, Pelin Telkoparan, "UNDERSTANDING THE CROSSTALK BETWEEN ENDOPLASMIC RETICULUM STRESS AND OXIDATIVE STRESS IN DISEASES" (2023). UBT International Conference. 12.
https://knowledgecenter.ubt-uni.net/conference/IC/PNS/12
UNDERSTANDING THE CROSSTALK BETWEEN ENDOPLASMIC RETICULUM STRESS AND OXIDATIVE STRESS IN DISEASES
UBT Lipjan, Kosovo
The endoplasmic reticulum (ER) is a vital organel with many critical cell functions. Various intracellular and environmental factors may disrupt its function and lead to the accumulation of unfolded or misfolded proteins that cause ER stress and activate the unfolded protein response (UPR). UPR leads to disruption of intracellular calcium and redox homeostasis and mitochondrial dysfunction. When the redox is unbalanced, the antioxidant mechanism is disrupted and leads to oxidative stress. ER stress mediates oxidative stress and increases reactive oxygen species (ROS) by affecting mitochondrial function, thus causing apoptosis in various metabolic diseases including cancer. In this talk, I will discuss how ER stress mediates oxidative stress in various metabolic diseases, including cancer, and the potential development of drugs that target these integrated signaling pathways.