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EIF4A3-induced circFAT1 promotes high glucose-induced podocyte damage via miR-30e-5p/SOX4 axis
Youqun Huang1,2, Yu Liu1, Mengfan Yang1
1Department of Nephrology, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China.
Insights
Circular RNA circFAT1 exacerbates diabetic nephropathy (DN) by promoting podocyte injury via the miR-30e-5p/SOX4 pathway. Inhibiting circFAT1 may offer a new therapeutic strategy for DN.
Area of Science:
- Molecular Biology
- Cell Biology
- Nephrology
Background:
- Podocyte injury is a key factor in diabetic nephropathy (DN) pathogenesis.
- Circular RNAs (circRNAs) are increasingly recognized as critical regulators in disease processes.
- circFAT1 (hsa_circ_0001461) has emerged as a potential player in pathological conditions.
Purpose of the Study:
- To investigate the role of hsa_circ_0001461 in high glucose (HG)-induced podocyte damage.
- To elucidate the underlying molecular mechanisms.
- To assess the clinical relevance of circFAT1 in diabetic nephropathy patients.
Main Methods:
- Studied circFAT1 expression in high glucose-induced podocyte injury models.
- Investigated the effects of circFAT1 inhibition on podocyte migration and differentiation.
- Utilized molecular techniques to explore the circFAT1/miR-30e-5p/SOX4 signaling pathway.
- Analyzed circFAT1 levels in patient samples.
Main Results:
- circFAT1 expression was significantly upregulated in podocytes under HG conditions.
- Inhibition of circFAT1 reduced podocyte migration and reversed epithelial-mesenchymal transition markers.
- circFAT1 was found to inhibit miR-30e-5p, leading to increased SOX4 expression.
- Elevated circFAT1 levels in DN patients correlated with disease severity (albuminuria, serum creatinine).
Conclusions:
- circFAT1 plays a critical role in high glucose-induced podocyte injury.
- The mechanism involves the circFAT1/miR-30e-5p/SOX4 signaling pathway.
- circFAT1 represents a potential therapeutic target for diabetic nephropathy intervention.
Abstract:
Podocyte injury significantly contributes to glomerular filtration dysfunction and albuminuria in diabetic nephropathy (DN). Circular RNAs, particularly circFAT1 (hsa_circ_0001461), have emerged as influential regulators in pathological processes. This research focused on exploring the function of hsa_circ_0001461 in high glucose (HG)-induced podocyte damage and the associated underlying mechanism. Here, we demonstrate that circFAT1 is significantly upregulated in HPCs under HG conditions. Inhibition of circFAT1 led to decreased podocyte migration and a restoration of differentiation markers, along with a reduction in mesenchymal markers. Mechanistically, circFAT1 was found to inhibit miR-30e-5p, resulting in enhanced SOX4 expression, which promoted epithelial-mesenchymal transition and migration in podocytes. Moreover, we identified EIF4A3 as a crucial regulator of circFAT1 biogenesis under hyperglycaemic conditions. Importantly, elevated levels of circFAT1 were also detected in DN patients, correlating with increased albuminuria and serum creatinine. In conclusion, this study elucidates the critical role of circFAT1 in HG-induced podocyte injury through the miR-30e-5p/SOX4 signalling pathway. The findings suggest that targeting circFAT1 May offer a potential strategy for DN intervention.
