Glutathione S-transferase mu 3 pseudogene 1 (GSTM3P1)

Glutathione S-transferase mu 3 pseudogene 1 (GSTM3P1) is a human pseudogene that does not encode a functional protein, but rather produces a long non-coding RNA (lncRNA). This lncRNA has a regulatory function rather than a catalytic or receptor activity. GSTM3P1 is upregulated in kidney proximal tubular cells following hypoxic or ischemic injury. It mediates acute kidney injury (AKI) in part by interacting with and promoting degradation of the microRNA mir-668, which under normal conditions has a protective effect on the kidney. Mechanistically, GSTM3P1 lncRNA binds to mir-668, triggering sequence-directed microRNA degradation, thus relieving suppression of pro-apoptotic pathways and increasing tubular cell death in the context of ischemia. In mouse models, knockout or knockdown of the homologous pseudogene Gstm2-ps1 reduces kidney injury, suggesting that targeting this lncRNA may have therapeutic potential for AKI[1][4]. GSTM3P1 is not a conventional therapeutic target such as an enzyme, receptor, or transporter. While upregulation of GSTM3P1 has been associated with kidney injury biomarkers like NGAL, GSTM3P1 itself is not a clinically used biomarker.

Other names

dJ984P4.2GSTM3Pglutathione S-transferase M3 pseudogeneglutathione S-transferase mu 3 (brain) pseudogeneGSTM3P1