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C/EBP⍺ Aggravated Ferroptosis and Apoptosis in Renal Tubular Epithelial Cell

ABSTRACT: C/EBP⍺ Aggravated Ferroptosis and Apoptosis in Renal Tubular Epithelial Cell

PROVIDER: PRJNA1014769 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25994100_1.fastq.gz	Fastqsanger.gz
	SRR25994100_2.fastq.gz	Fastqsanger.gz
	SRR25994101_1.fastq.gz	Fastqsanger.gz
	SRR25994101_2.fastq.gz	Fastqsanger.gz
	SRR25994102_1.fastq.gz	Fastqsanger.gz

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C/EBP⍺ Aggravated Ferroptosis and Apoptosis in Renal Tubular Epithelial Cell

Project description:Acute Kidney Injury (AKI) is widely recognized for its rapid deterioration in renal function, often resulting in unfavorable clinical outcomes. An increase in the expression of CCAAT/enhancer binding protein alpha (C/EBP⍺) has been observed in both human and mouse kidneys affected by AKI. We unraveled the downstream pathway of C/EBP⍺ through RNA-sequencing, confirming our findings with qRT-PCR and luciferase reporter assays. Furthermore, we identified a potential target for AKI reversal in a murine AKI model.

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Project description:Ferroptosis is an iron-dependent programmed cell death associated with severe kidney diseases, linked to decreased glutathione peroxidase 4 (GPX4). However, the spatial distribution of renal GPX4-mediated ferroptosis and the molecular events causing GPX4 reduction during ischemia-reperfusion (I/R) remain largely unknown. Using spatial transcriptomics, we identify that GPX4 is situated at the interface of the inner cortex and outer medulla, a hyperactive ferroptosis site post-I/R injury. We show that OTU deubiquitinase 5 (OTUD5) is a GPX4-binding protein that confers ferroptosis resistance by stabilizing GPX4. During I/R, ferroptosis is induced by mTORC1-mediated autophagy, causing OTUD5 degradation and subsequent GPX4 decay. Functionally, OTUD5 deletion intensifies renal tubular cell ferroptosis and exacerbates acute kidney injury, while AAV-mediated OTUD5 delivery mitigates ferroptosis and promotes renal function recovery from I/R injury. In this work, our study highlights a new autophagy-dependent ferroptosis module: hypoxia/ischemia-induced OTUD5 autophagy triggers GPX4 degradation, offering a potential therapeutic avenue for I/R-related kidney diseases.

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