In high glucose-stimulated human renal tubular epithelial cells (HK-2), MALAT1 knockdown alleviated cell viability inhibition, apoptosis, and inflammatory responses, effects that were reversed by a miR-15b-5p inhibitor or TLR4 overexpression, indicating that MALAT1 promotes DKD progression via the miR-15b-5p/TLR4 signaling axis. This evidence concerns the gene TLR4 and diabetic kidney disease.