Review Article

MicroRNAs Involved in the Lipid Metabolism and Their Possible Implications for Atherosclerosis Development and Treatment

Table 2

Additional microRNAs involved in the lipid metabolism and atherosclerosis.

MicroRNATarget mRNAFunctionReference

miR-1/206LXRαSuppresses lipogenesis.[24]

miR-9ACAT1Decreases formation of foam cells.[25]
PPARδMediates inflammatory response in human monocytes following lipopolysaccharide treatment.[26]

miR-21FABP7Downregulated in the livers of mice on a high-fat diet. MiR-21 levels may be upregulated by lycopene, thus blocking lipid accumulation.[27]

miR-29aLPLUpregulated in oxLDL-treated dendritic cells. By targeting LPL, it affects lipid uptake and inflammatory cytokine secretion.[28]

miR-30cMTPReduces ApoB secretion, lipid synthesis, and atherosclerosis in ApoE−/− mice.[29]

miR-125a-5pORP9Upregulated in macrophages treated with oxLDL mediating lipid uptake. Inhibits the secretion of inflammatory cytokines (IL-2, IL-6-, TNFα, TGFβ).[30]

miR-155SCG2Upregulated in oxLDL-treated macrophages/dendritic cells. Important for lipid uptake and expression of adhesion molecules.[31]
LXRαUpregulated in the liver of animals on a high-fat diet. Upregulation seems to protect them from steatosis, since miR-155−/− animals are susceptible to hepatosteatosis.[32]
FADDAttenuates oxLDL-mediated macrophage apoptosis implicating a possible protective role in atherosclerosis.[33]

miR-181bImportin-α3Downregulated in ApoE−/− mice and in subjects with CAD. Delivery of miR-181b reduces inflammatory response and protects ApoE−/− mice from atherosclerosis.[34]

miR-185/342SREBPIn prostate cancer cells, miR-185 and miR-342 target SREBP, causing FASN and HMGCoAR downregulation.[35]

miR-217SIRT1Upregulated in the liver of chronically ethanol-fed mice, resulting in fat accumulation.[36]

miR-335–-Upregulated in the liver and white adipose tissue of obese mice. During adipose tissue differentiation, its levels correlate with lipid accumulation and e.g., PPARγ or FAS levels.[37]

miR-378/378*CRAT, MED13Both miRNAs are encoded within the PGC-1β gene which is important for mitochondrial development and metabolism. By targeting CRAT and MED13, they affect fatty acid metabolism and metabolic gene expression control.[38]
–-Overexpression of miR-378/378* stimulates lipogenesis and increases lipid droplet size in developing adipocytes.[39]

miR-467b LPLDownregulated in the liver of high-fat diet-fed mice, which results in the upregulation of LPL and affects the development of hepatosteatosis.[40]
Decreased lipid accumulation and inflammatory cytokine secretion in oxLDL-treated macrophages.[41]

miR-613LXRαSuppresses lipogenesis.[42]

LXRα: liver X receptor; ACAT1: acyl-coenzyme A: cholesterol acyltransferase; PPARγ: peroxisome proliferator-activated receptor γ; FABP7: fatty acid-binding protein 7; LPL: lipoprotein lipase; MTP: microsomal triglyceride transfer protein; ORP9: oxysterol binding protein-like 9; SCG2: secretogranin 2; FADD: fas-associated death domain-containing protein; SREBP: sterol regulatory element binding protein; SIRT1: sirtuin 1; CRAT: carnitine O-acetyltransferase; MED13: mediator of RNA polymerase II transcription subunit 13; oxLDL: oxidized low-density lipoprotein.