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TET 2 Deficiency Exacerbates Podocyte Injury and Mitophagy Disorder in Diabetic Nephropathy by Regulating M 5 C Methylation of Bcas3
Lack of TET2 worsens kidney cell damage and mitochondrial recycling problems in diabetic kidney disease by changing RNA modifications of Bcas3
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Abstract
A marked increase in 5-methylcytidine (m5C) levels was observed in the kidneys of type 2 diabetic mice.
- Increased m5C levels in diabetic kidneys were associated with reduced expression of the m5C demethylase TET2.
- Decreased TET2 expression in renal biopsy samples from diabetic nephropathy patients correlated with impaired renal function.
- Overexpression of TET2 in high glucose-stimulated podocytes enhanced mitophagy and reduced cell injury.
- Systemic delivery of AAV-TET2 in diabetic mice led to reduced albuminuria and improved kidney histopathology.
- TET2 influences mitophagy by modulating the m5C methylation of Breast Carcinoma Amplified Sequence 3 (Bcas3), which also promotes mitophagy.
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