Table 1.

Table showing the research studies completed on different miRNAs and lncRNAs and the underlying mechanism.

ncRNA	Cells Involved	Animal Model Used	Genes Downregulated/Upregulated	Mechanism	Pathway Activated	Reference
miR-122	HepG2 and Huh-7 cells	16 C57BL/6 mice (males, 8 weeks old)	Downregulation of Sirt1	Binds to 3′-UTR and substantial mRNA degradation downregulates sirt1.	AMPK pathway	[146]
miR-21	CD45+ cells, T cells	Eight-week-old male Ldlr−/− mice, nine-week-old male WT or miR-21−/− mice	Downregulation of ß-oxidation genes Cpt1 and Acox1	Through normalizing liver PPARα, miR-21 inhibition and suppression significantly reduced liver damage, inflammation, and fibrogenesis.	PPARα pathway	[84]
miR-34a	Kupffer cells	miR-34afl/fl mice, albumin-Cre (Alb-Cre) mice, and C57BL/6J mice	Induces (Cyp7a1 and Cyp8b1)	miR-34a promotes the induction of Kupffer cell activation/inflammation, lipotoxicity, and apoptosis; boosts CYP7A1 and CYP8B1 expression, which causes a temporary drop in free cholesterol (FC) levels and the subsequent induction of SREBP2 processing and its target genes, including HMGCR. It enhances the conversion of FC to bile acids.	miR-34a-sirtuin 1 (SIRT1)-SREBP1c pathway activates hepatic TGFb signaling,	[147]
miR-192	HepG2 cells	Male C57BL/6 mice	Downregulation of SREBF1 target genes, including FASN and PPARG i	miR192 acts directly on the 3′UTR of SREBF1, which results in the dysregulation of lipid homeostasis in the hepatocytes.	Suppress SBREPF1	[148]
lncRNA MALAT1	HepG2 and AR42J	Male C57BL/6 mice (8 weeks old, n = 6/group)	---------	PPARα expression was significantly increased, and CD36 levels were significantly decreased when MALAT1 was knocked down.	MALAT1 could regulate PPARα/CD36 through the mediation of the miR-206/ARNT axis	[115]
lncRNA HOTAIR	HepG2 cells	Adult (8-week-old) male C57BL/6J mice	HOTAIR knockout increases the expression of genes	HOTAIR enhances the accumulation of PRC2 and H3K27 trimethylation to the MEG3 promoter	Regulates the expression of the DNMT1/MEG3/p53 pathways	[117]
lncRNA APTR	Hepatic stellate cells	(CCl4)-treated mice	Attenuates TGFB1-induced upregulation of ACTA2	The overexpression of α-SMA in HSCs brought on by TGF-β1 is prevented by suppressing APTR.	Abrogate TGF-β1-induced upregulation of α-SMA	[69,149]
lncRNA PVT1	Primary HSCs cells	Eight-week-old male C57BL/6J mice	Regulates the expression of PTCH1, SMO, and GLI2	Chromatin modification, transcriptional regulation, and post-transcriptional regulation	PVT1 silencing inhibits the Hh pathway	[150]
lncRNA COX2	IEC cell line (IEC4.1)	C57BL/6J mice	Enhances the transcription of Il12b	By controlling Mi-2/NuRD-mediated epigenetic histone changes, LincRNA-Cox2 affects the transcription of the Il12b gene in intestinal epithelial cells stimulated by TNF.	Activates NF-ĸB signaling pathway	[126]
lncRNA NEAT 1	HepG2 cells and LO2 cells	------	Activates lipogenesis-related genes, such as ACC and FAS	By targeting miR-139-5p, NEAT1 knockdown reduces lipid buildup in the NAFLD cellular model.	Regulates the c-Jun/SREBP1c pathway	[151]
lncRNA UC372	HepG2 cells	C57BL/6J mice	Regulates the expression of genes related to lipid synthesis and uptake, including ACC, FAS, SCD1, and CD36	By inhibiting miR-195/miR-4668 maturation from reversing miR-195/miR-4668-mediated suppression of functional target gene expression, uc.372 promotes hepatic steatosis.	-----	[135]
lncARSR	human HCC cells (HepG2)	C57BL/6 male mice (aged 6 weeks)	-------	lncARSR inhibits YAP1, which inhibits phosphorylation nuclear translocation	Suppresses IRS2/AKT pathway	[31]
lncRNA APOA4-AS	Primary hepatocytes cells	C57BL/6 mice	Decreases APOA4 mRNA and protein levels, whereas expression of other lipid metabolism-associated genes (e.g., FASN, SCD1, APOB, MTP, CPT1α, and MCAD) were not altered	HuR, a protein that stabilizes mRNA, and APOA4-AS interact to stabilize APOA4 mRNA.	Regulates many metabolic pathways	[76]
lncRNA H19	HepG2 and Huh-7 cells	C57BL/6 mice (males, 8 weeks old)	H19 and PPARγ were upregulated	H19 exerts its biological functions in NAFLD by using a ceRNA mechanism to control the expression of miR-130a’s downstream genes.	Regulates miR-130a/PPARγ pathway	[152]