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FoxO3a: capture the bond between magnesium and diabetic kidney disease
Taoran Chen1, Miao Sun1, Qi Zhou2
1Department of Laboratory Medicine, First Hospital of Jilin University, Changchun, China.
Abstract:
Hyperglycemia in Diabetic Kidney Disease (DKD) induces excessive accumulation of reactive oxygen species (ROS) through various pathways, leading to oxidative stress, ferroptosis, and mitochondrial dysfunction, which collectively contribute to kidney damage. Currently, the treatment of DKD remains a significant challenge. Magnesium, an essential mineral, has emerged as a promising therapeutic agent for DKD due to its anti-inflammatory and antioxidant properties. Magnesium has been shown to alleviate renal fibrosis, maintain tubular integrity and function, improve endothelial cell function, and regulate renal hemodynamics. As a cofactor of antioxidant enzymes, Magnesium directly scavenges ROS and enhances the expression of antioxidant proteins. This review explores the relationship between Magnesium and DKD, examining how Magnesium mitigates oxidative stress through the PI3K/AKT/FoxO3a pathway, inhibits ferroptosis in renal tubular epithelial cells via the AMPK/FoxO3a/Nrf2 pathway, and reduces autophagy and apoptosis, thereby delaying DKD progression. The review further discusses how Magnesium regulates the pivotal FoxO3a protein, a transcription factor with antioxidant properties, leading to the prevention of DKD, and proposes Magnesium supplementation as a potential clinical strategy for alleviating DKD, offering a new therapeutic approach for its treatment.
Insights
Magnesium effectively combats diabetic kidney disease (DKD) by reducing oxidative stress and cell death. Supplementation shows promise for treating DKD and preventing kidney damage.
Area of Science:
- Biochemistry
- Nephrology
- Molecular Biology
Background:
- Diabetic kidney disease (DKD) involves hyperglycemia-induced oxidative stress, ferroptosis, and mitochondrial dysfunction, leading to kidney damage.
- Current DKD treatments face significant challenges.
- Magnesium, an essential mineral, exhibits antioxidant and anti-inflammatory properties beneficial for DKD.
Purpose of the Study:
- To review the role of magnesium in mitigating oxidative stress, ferroptosis, and apoptosis in DKD.
- To explore magnesium's mechanisms of action, including its regulation of key signaling pathways.
- To evaluate magnesium supplementation as a potential therapeutic strategy for DKD.
Main Methods:
- Literature review of studies investigating magnesium's effects on DKD.
- Analysis of molecular pathways, including PI3K/AKT/FoxO3a and AMPK/FoxO3a/Nrf2.
- Examination of magnesium's impact on reactive oxygen species (ROS) scavenging and antioxidant protein expression.
Main Results:
- Magnesium alleviates renal fibrosis, preserves tubular integrity, improves endothelial function, and regulates renal hemodynamics.
- Magnesium mitigates oxidative stress via the PI3K/AKT/FoxO3a pathway.
- Magnesium inhibits ferroptosis in renal tubular epithelial cells through the AMPK/FoxO3a/Nrf2 pathway, reducing autophagy and apoptosis.
Conclusions:
- Magnesium plays a crucial role in preventing DKD by regulating the antioxidant transcription factor FoxO3a.
- Magnesium directly scavenges ROS and enhances antioxidant defenses.
- Magnesium supplementation presents a promising therapeutic avenue for managing and treating DKD.
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