Table 1.
Relevant miRNAs in oxidative stress response.
ROS source/pathology | miRNAs upregulated | Tissue/organ | Source | Target | Functions | References |
---|---|---|---|---|---|---|
H2O2 | miR-200c miR-141 miR-200a miR-200b miR-429 |
endothelium, myoblasts | Human | ZEB1 | apoptosis, senescence | [22] |
H2O2 | miR-200c miR-141 miR-200a miR-200b miR-429 |
ovarian adenocarcinomas | Human | p38α | ROS accumulation; improved response to chemotherapy | [25] |
H2O2 | miR-200c | primary hippocampal neurons | Mouse | Unknown | Unknown | [26] |
chronic H2O2 treatment | miR-200c | trabecular meshwork cells | Human | Unknown | senescence | [27] |
t-BHP | miR-200c miR-141 | auditory cells | Mouse | Unknown | Unknown | [28] |
Obesity | miR-200c miR-141 | Heart | Rat | S6K1 | compensatory/adaptive mechanisms | [29] |
Diabetes | miR-200c miR-141 | Heart | Mouse | Slc25a3 | dysregulation ATP production; cell death | [30] |
Diabetes | miR-200c miR-200b miR-429 |
VSMCs | Mouse | ZEB1 | inflammation | [31] |
NO | miR-200c miR-200a miR-200b miR-429 |
mES | Mouse | ZEB2 | mesendoderm and cardiovascular differentiation | [32] |
Hypoxia/ROS | miR-210 | ASCs | Human | PTPN2 | proliferation, migration | [33] |
Hypoxia | miR-210 | ECs, breast and colon cancer cells | Human | ISCU1/2 | mitochondrial respiration | [34–36] |
Hypoxia | miR-210 | breast cancer cells | Human | TfR1 | mitochondrial respiration; proliferation | [37] |
Hypoxia | miR-210 | H9c2 Cardiomyocytes | Mouse | FECH | heme biosynthesis; Iron homeostasis | [38] |
Hypoxia | miR-210 | colon, breast, esophageal cancer cells | Human | COX10 | mitochondrial respiration; ROS production | [39] |
Hypoxia | miR-210 | lung cancer cells | Human | SDHD | mitochondrial respiration; proliferation | [40] |
Hypoxia | miR-210 | ovarian cancer cells | Human | NDUFA4 | mitochondrial respiration | [41] |
Diabetes | miR-125 | VSMCs | Mouse | Suv39h1 | inflammation | [42] |
Obesity | miR-27 | Adipose tissue | Mouse | PPARγ, C/EBPα | inflammation | [43] |
H2O2 | miR-21 | VSMCs | Rat | PDCD4 | apoptosis protection | [44] |
Coronary artery disease | miR-21 | APCs | Human | SOD-2 SPRY-1 | ROS production; APC migratory defects | [45] |
Atherosclerosis | miR-217 | Atherosclerotic plaques | Human | SIRT-1 | endothelial dysfunction | [46] |
Myocardial infarction | miR-34 | BMCs | Human | SIRT-1 | apoptosis | [47] |
Mitochondrial dysfunction | miR-23a/b | B lymphoma, prostate cancer cells | Human | Mitochondrial GLS | ROS production | [48] |
Mitochondrial dysfunction | miR-15 family, miR-424 | Cardiomyocytes | Rat | Arl2 | ATP reduction | [49] |
downregulated: | ||||||
Obesity | miR-155 miR-183 miR-872 |
Adipose tissue | Rat | HO-1 | inflammation, oxidative damage, apoptosis | [50] |
Hypoxic preconditioning | miR-199a | Cardiomyocytes | Rat | SIRT-1 | apoptosis protection | [51] |
H2O2 | miR-23a/b | Retinal pigment epithelial cells | Human | Fas | apoptosis | [52] |