Expression and mechanism exploration of lncRNA MALAT1 in children with IgA vasculitis nephritis.

IgA vasculitis (IgAV) is the most common systemic small vessel vasculitis in children. Renal involvement is called IgA vasculitis nephritis (IgAVN) and represents one of the most severe complications of this disease. The primary objective of this study was to evaluate the abnormal expression of Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) in IgAVN and to elucidate its involvement in the underlying pathogenic mechanisms by regulating the miR-142-3p/SYK axis. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was employed to quantify MALAT1 expression levels. A dual-luciferase reporter assay was used to verify the targeting relationships among MALAT1, miR-142-3p, and SYK. The in vitro functional effects of MALAT1 and miR-142-3p on cell proliferation and apoptosis were assessed using CCK-8 assays and detection of apoptotic markers. Simultaneously, an enzyme-linked immunosorbent assay (ELISA) was utilized to analyze the levels of inflammatory factors. MALAT1 and SYK were significantly upregulated in IgAVN patients, whereas miR-142-3p was downregulated. MALAT1 exhibited potential in distinguishing IgAVN patients from those with IgAV without renal involvement. Furthermore, knockdown of MALAT1 inhibited excessive proliferation, promoted apoptosis, and alleviated the inflammatory response of human glomerular mesangial cells (HGMCs) induced by angiotensin II (Ang II) through regulation of the miR-142-3p/SYK axis. MALAT1 may be a biomarker of IgAVN, and the MALAT1/miR-142-3p/SYK axis may become a therapeutic target for IgAVN.