Key result
Elevated plasma hsa_circ_0004662 expression links to NASH and NASH-associated liver fibrosis.
Why the study?
The diagnostic performance of current non-invasive biomarkers for NAFLD remains suboptimal, while circRNAs have emerged as potential biomarkers and therapeutic targets.
Does hsa_circ_0004662 serve as a diagnostic biomarker and promote disease progression in NAFLD?
Case-Control (n=261)
Does hsa_circ_0004662 serve as a diagnostic biomarker and promote disease progression in NAFLD?
hsa_circ_0004662 is upregulated in NAFLD progression and may serve as a diagnostic biomarker and therapeutic target by promoting lipid accumulation and fibrosis via miR-532-3p interaction.
May support hsa_circ_0004662 as NASH biomarker; leaves open therapeutic targeting pending human trials.
Objectives Non-alcoholic fatty liver disease (NAFLD) is a progressive disease. The diagnostic performance of current non-invasive biomarkers for NAFLD remains suboptimal. Circular RNAs (circRNAs) have emerged as potential biomarkers and therapeutic targets due to their involvement in disease progression. This study investigated the diagnostic potential and underlying mechanisms of hsa_circ_0004662 in NAFLD. Methods The study combined bioinformatics and experimental approaches. Analysis of the GSE134146 dataset revealed differentially expressed circRNAs, leading to RT-qPCR verification of hsa_circ_0004662 in clinical cohorts. Cellular models were utilized to assess triglyceride (TG) content in HepG2 cells and fibrosis markers in LX-2 cells; potential miRNA interactions were examined through integrated prediction and validation. Results Screening of the GSE134146 dataset revealed that hsa_circ_0004662 was the most markedly upregulated circRNA. This finding was confirmed in our independent clinical cohort, comprising 156 NAFLD patients and 105 healthy controls. Compared with healthy controls, the expression of hsa_circ_0004662 was gradually upregulated in plasma samples of patients with non-alcoholic steatohepatitis (NASH) and NASH-associated liver fibrosis (NASH-AF). hsa_circ_0004662 promoted lipid accumulation in HepG2 cells and fibrosis in LX-2 cells. Mechanistically, hsa_circ_0004662 likely interacts with miR-532-3p to promote NAFLD. Conclusions Hsa_circ_0004662 holds potential as a non-invasive diagnostic biomarker and therapeutic target for NAFLD. Further validation and mechanistic studies are warranted to elucidate its role in disease progression.
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Lin et al. (2026) conducted a case-control in Non-alcoholic fatty liver disease (NAFLD) (n=261). hsa_circ_0004662 vs. Healthy controls was evaluated on hsa_circ_0004662 expression in plasma samples. Expression of hsa_circ_0004662 was gradually upregulated in plasma samples of patients with NASH and NASH-associated liver fibrosis compared with healthy controls.
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