I am just wondering the relationship of ROS generation and HIF1a expression. HIF1a will be activated by hypoxia and ROS will also generate in the same condition. What if there is extracellular ROS provided to the cell?
Hypoxia induces HIF expression. This leads to a metabolic switch in which the cell adopts a glycolytic phenotype.
Glycolysis decreases the production of ROS while OXPHOS increases it.
The glycolytic pathway coexists with an increased Pentose Phosphate Pathway which produces NADPH that regenerates antioxidant compounds like thioredoxin. In this manner ROS are neutralized.
Hello,
Thank you for this question, this is an interesting topic of study.
ROS production increases in hypoxia and, in fact, ROS production presents a biphasic curve, with high production rate under hypoxia and hyperoxia.
Regarding HIF1α, I would like you to consider HIF1α stabilization rather than expression. HIF1α is kept under low levels during normoxia due to the activity of prolyl hydroxylase enzymes. These enzymes use molecular oxygen to hydroxylate HIF-1α on two conserved proline residues (Pro(402) and Pro(564)). It has been demonstrated that ROS can directly inhibit these enzymes, therefore, resulting in the stabilization of HIF1α. It is possible to speculate that this ROS action on HIF1α stabilization is related to the antioxidant response (increase on antioxidant defense) after ROS exposure or redox stress.
Best regards,
Henver
Yes ROS can induce mitochondrial damage, resulting in activation of autophagy-related glycolysis mediated by HIF1a.
Please read my article:
Article Upregulation of autophagy and glycolysis markers in keloid h...
Best regards
Nabil
- Badges
- Science method
- Similar topics
- Biological Science
- Histology
- Staining