Division of Gastroenterology, The First Affiliated Hospital of Kunming Medical University, Kunming, 650031, People's Republic of China.
Transfusion Medicine Research Department, Yunnan Kunming Blood Center, Kunming, 650011, People's Republic of China.
Clin Exp Med. 2020 Nov;20(4):587-600. doi: 10.1007/s10238-020-00636-1. Epub 2020 Jun 3.
Longitudinal studies have improved current diagnostics and management of metabolic associated fatty liver disease (MAFLD) patients by liver biopsy and therapeutic intervention, yet the deficiency of biomarker spectrum for dissecting subtypes largely hinders the symptomatic treatment. We originally enriched serum from peripheral blood of 618 healthy donors (HD) and 580 MAFLD (400 NAFL, 180 NASH) patients according to multiple clinicopathological indicators. Microarray profiling and qRT-PCR were conducted to identify lncRNAs as candidate biomarkers of MAFLD. Then, we analyzed the matching score of the indicated lncRNA with CAP or MAFLD-associated pathological parameters as well. Additionally, we took advantage of interaction network together with gene expression profiling analysis to further explore the underlying target genes of the identified lncRNA. Herein, we found CAP in nearly all of the NAFL (399/400) and NASH (179/180) patients was higher than that in the HDs (611/618). The differentially expressed lncRNAs were involved in multiple metabolic or immunologic processes by regulating MAFLD-associated pathways. Of them, serum lncPRYP4-3 was identified as a novel candidate biomarker of MAFLD, which was further confirmed by correlation analysis with clinical indicators. Thereafter, we deduced PRS4Y2 was a candidate target of lncPRYP4-3 and mediated the dysfunction in NAFL and NASH patients. Serum lncPRYP4-3 served as a novel biomarker of MAFLD and helped distinguish the subtypes and benefit precise intervention therapy. Our findings also provided overwhelming new evidence for the alteration in biological processes and gene ontology in MAFLD patients.
纵向研究通过肝活检和治疗干预改善了代谢相关脂肪性肝病 (MAFLD) 患者的当前诊断和治疗,但生物标志物谱的缺乏在很大程度上阻碍了症状治疗。我们最初根据多种临床病理指标从 618 名健康供体 (HD) 和 580 名 MAFLD (400 名非酒精性脂肪肝,180 名非酒精性脂肪性肝炎) 患者的外周血中富集血清。通过微阵列分析和 qRT-PCR 鉴定 lncRNA 作为 MAFLD 的候选生物标志物。然后,我们分析了指示性 lncRNA 与 CAP 或 MAFLD 相关病理参数的匹配分数。此外,我们利用相互作用网络和基因表达谱分析进一步探讨了鉴定出的 lncRNA 的潜在靶基因。在此,我们发现几乎所有的非酒精性脂肪肝 (399/400) 和非酒精性脂肪性肝炎 (179/180) 患者的 CAP 都高于 HDs (611/618)。差异表达的 lncRNA 通过调节 MAFLD 相关途径参与多种代谢或免疫过程。其中,血清 lncPRYP4-3 被鉴定为 MAFLD 的一个新的候选生物标志物,通过与临床指标的相关性分析进一步得到证实。此后,我们推断 PRS4Y2 是 lncPRYP4-3 的候选靶基因,并介导了非酒精性脂肪肝和非酒精性脂肪性肝炎患者的功能障碍。血清 lncPRYP4-3 是 MAFLD 的一个新的生物标志物,有助于区分亚型并有利于精确的干预治疗。我们的研究结果还为 MAFLD 患者的生物学过程和基因本体改变提供了压倒性的新证据。