Diagnostic Value and Mechanism of Action of LINC00641 in Sepsis-Associated Acute Kidney Injury

Purpose: Sepsis-associated acute kidney injury (SAKI) has a rapid onset and carries serious risks. Long non-coding RNAs (lncRNAs) appear to have a key role in SAKI pathogenesis. The goal of this study is to explore the expression and molecular mechanisms of LINC00641 in patients with SAKI. Patients and Methods: Clinical data between SAKI and sepsis-only patients were compared using analysis of variance. Serum LINC00641 and miR-485-5p levels were measured by qRT-PCR. The predictive value of LINC00641 for SAKI was evaluated with ROC curves. Cell Counting Kit-8, flow cytometry, qRT-PCR and enzyme-linked immunosorbent assay were used to assess cell proliferation, apoptosis, apoptosis-related mRNA, and inflammatory factor level. Dual luciferase and RNA immunoprecipitation assays were used to validate the LINC00641-miR-485-5p interaction. Results: SAKI patients exhibited significantly elevated serum levels of LINC00641 compared to non-SAKI patients. The ROC analysis confirmed that LINC00641 possesses strong diagnostic potential for SAKI. Reducing LINC00641 expression mitigated LPS-induced damage to renal epithelial cells, marked by enhanced cell proliferation, reduced apoptosis, and lower levels of IL-6 and TNF-α. In SAKI patients, serum miR-485-5p levels were inverse linked to LINC00641 expression. Suppression of miR-485-5p expression abrogated the protective benefits of reduced LINC00641 expression on renal epithelial cell injury. Conclusion: Elevated serum expression of LINC00641 is tightly linked to the emergence and progression of SAKI. By modulating the expression of miR-485-5p, LINC00641 influences LPS-induced renal epithelial cell injury, suggesting a novel therapeutic target for SAKI.