Fig. 9: Schematic illustrating the regulatory role of RSDR in ferroptosis during AKI. | Nature Communications

Fig. 9: Schematic illustrating the regulatory role of RSDR in ferroptosis during AKI.

From: The long non-coding RNA RSDR protects against acute kidney injury in mice by interacting with hnRNPK to regulate DHODH-mediated ferroptosis

Fig. 9: Schematic illustrating the regulatory role of RSDR in ferroptosis during AKI.

Upon AKI stimulation, RSDR expression is downregulated. RSDR normally functions to restrict the nuclear export of hnRNPK, thereby facilitating its nuclear accumulation and promoting the transcription of DHODH. DHODH maintains mitochondrial redox homeostasis and suppresses lipid peroxidation. Loss of RSDR impairs this regulation, leading to DHODH reduction, enhanced mitochondrial lipid peroxidation, and ferroptosis. These changes contribute to tubular injury and AKI progression. Together, this pathway highlights a lncRNA–protein–mitochondrial axis that links epigenetic control and cell death regulation in renal pathophysiology.

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