miR-93

更新于：2025-05-07

基本信息

别名

hsa-mir-93、microRNA 93、MIR93

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简介-

关联

100 项与 miR-93 相关的临床结果

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100 项与 miR-93 相关的转化医学

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0 项与 miR-93 相关的专利（医药）

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933

项与 miR-93 相关的文献（医药）

2025-08-01·Metabolism

Hepatic miR-93 promotes the pathogenesis of metabolic dysfunction-associated steatotic liver disease by suppressing SIRT1

Article

作者: Yun, Hwayoung ; Lee, Jinyoung ; Kim, Won Kon ; Hwang, Seonghwan ; Park, Neung Hwa ; Yang, Yong Ryoul ; Kim, Kimyeong ; Ryu, Dongryeol ; Kwon, Yuseong ; Lee, Ji Young ; Lee, Tae Young ; Nam, Dougu ; Ji, Haneul ; Lee, Haeseung ; Kim, Kwangho ; Dao, Tam ; Park, Kieun ; Choi, Jang Hyun ; Kim, Misung ; Khim, Keon Woo ; Kim, Ji Won ; Lee, Yo Han ; Baik, Bukyung ; Jeong, Joonho ; Yoon, Haejin

BACKGROUND AND AIMSThe molecular mechanisms underlying metabolic dysfunction-associated steatotic liver disease (MASLD) remain largely unclear; however, emerging evidence suggests that microRNAs (miRNAs) play a critical role in modulating transcriptional regulation of target genes involved in MASLD. This study aims to elucidate the role of miR-93 in lipid metabolism and MASLD progression.METHODSWe comprehensively analyzed miRNA expression profiles in liver tissues from patients with MASLD and diet-induced obese mice. miR-93 knockout (KO) mice were fed a high-fat-high-fructose (HFHFr) diet to assess the impact of miR-93 deficiency on MASLD. Transcriptome analysis was performed to elucidate the molecular mechanisms and role of miR-93 in MASLD. Additionally, we employed a high-throughput screening system to identify drugs capable of modulating miR-93 expression.RESULTSmiR-93 was significantly upregulated in the livers of patients with MASLD and diet-induced obese mice. miR-93 KO mice exhibited reduced hepatic steatosis. Specifically, miR-93 deficiency upregulated genes involved in fatty acid oxidation and downregulated genes associated with cholesterol biosynthesis. Sirtuin 1 (SIRT1) was identified as a direct target of miR-93, and miR-93 KO enhanced SIRT1 expression and activated the LKB1-AMPK signaling pathway. Niacin treatment downregulated miR-93, ameliorating hepatic steatosis by enhancing SIRT1 activity.CONCLUSIONSThese findings implicate miR-93 as a novel therapeutic target for MASLD. The study demonstrates the therapeutic potential of niacin in modulating the miR-93/SIRT1 axis, providing a new potential treatment for MASLD, a disease with limited current treatment options.

2025-03-04·Journal of Immunoassay and Immunochemistry

Estimate of circRNAs and microRNAs synergies on clinical advance of psoriasis

Article

作者: EL-Naidany, Sherin S. ; Tayel, Safaa I. ; Saleh, Amany A. ; El-Masry, Eman A. ; Shehata, Wafaa A. ; Abd-Elhafiz, Huda I. ; Elhelbawy, Mohammed G.

BACKGROUNDNoncoding RNAs have recently proven their contributing role in the pathogenesis of numerous diseases. The etiology of psoriasis is still not well defined, and genetic and environmental factors are blamed. We meant to explore the association of circRNAs/microRNAs in psoriasis and inspect their correlation with the clinical features of the disease.DESIGN AND METHODSThis study included 166 subjects: 83 cases with plaque psoriasis and 83 age- and sex-matched healthy persons as the control group. The expression levels of circRNA000102, circRNA0045272, circRNA0084764, and microRNAs -93,181, 16a, and 21 were estimated by quantitative real-time PCR.RESULTSCircRNA0045272 was ten-fold up-regulated, whereas circRNA0084764 and circRNA000102 were about two-fold downregulated in patients vs. control. MicroRNAs -93 and 181 were significantly downregulated in patients vs. control, whereas microRNA -16a and 21 were up-regulated in patients vs. control. CircRNA0045272 was positively correlated with microRNA 181, and circRNA0084764 was positively correlated with microRNA 93 and microRNA 181. CircRNA0045272 had the highest sensitivity (98.8%) and specificity (93.98%), and microRNA-16a had sensitivity (98.80%) with specificity (93.98%).CONCLUSIONWe assume that circRNAs can predict psoriasis occurrence and progression by sponging a set of microRNAs and can modulate several genes that disturb immune cell balance and inflammatory elements in psoriasis.

2025-03-01·Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

Exosomes derived from fibroblasts in DFUs delay wound healing by delivering miR-93-5p to target macrophage ATG16L1

Article

作者: Gao, Weicheng ; Yi, Min ; Zhao, Liping ; Tu, Liying ; Wu, Guoping ; Zhang, Lantian ; Xu, Zibo ; Lin, Jinde ; Zhang, Qian ; Ni, Tianyi ; Yan, Wei ; Sun, Xiaowei

Diabetes is an extremely costly disease, one-third of which are attributed to the management of diabetic foot disease including chronic, non-healing, diabetic foot ulcers (DFUs). Therefore, much effort is needed to understand the pathogenesis of DFUs and novel therapeutics. We utilized exosome staining to confirm the interaction between fibroblast-derived exosomes and macrophages. Subsequently, we employed public data and qPCR to screen for upregulated miRNAs in fibroblast-derived exosomes in DFUs. The relationship between was validate miR-93-5 and ATG16L1 through data prediction and dual-luciferase reporter assays. A variety of molecular biology experiments were used for subsequent pathway validation. Additionally, we established Atg16l1^MKI and Nlrp3^MKO mice for further validation. We identified that miR-93-5p derived from fibroblasts played an important role in M1 macrophages polarization. Predicted by database, we found that miR-93-5p can bind to ATG16L1 mRNA, thereby influencing macrophage autophagy mediated by ATG16L1 in the clearance of ROS, thus activating the NLRP3 signaling pathway. In vivo, miR-93-5p antagomir treatment accelerated diabetic wound healing and induced M2 macrophage polarization. Fibroblasts and macrophages show cell crosstalk during the development of DFUs by miR-93-5p, and that antagomir treatment may be a promising and technically advantageous alternative to DFUs therapies.

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