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

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.

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.

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.

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.