| mir-124 | — | Loss of mir-124 increases reactive oxygen species formation and accumulation of the aging marker lipofuscin, reduces whole body ATP levels and results in reduction in lifespan [23075628].
Supplementation of vitamin C normalizes the reduced median lifespan of mir-124 mutants [23075628].
The expression of the conserved mir-124 in whole wrn-1 mutants (which premature age) is significantly reduced [23075628]. | Nematode |
| mir-58 | — | mir-58(n4640) mutation decreases the mean lifespan by 20% [22482727]. | Nematode |
| mir-239 | — | Mutating mir-239 increases mean and maximum lifespan by 12 and 36%, respectively, whereas overexpressing mir-239 decreases mean and maximum lifespan by 13 and 17 - 33%, respectively [21129974]. | Nematode |
| mir-246 | — | Mutating mir-246 decreases mean and maximum lifespan by 12%, while its overexpression increases mean and maximum lifespan by 6 and 5 - 14%, respectively [21129974]. | Nematode |
| mir-238 | — | Mutating mir-238 decreases mean and maximum lifespan by 18 and 24% [21129974]. mir-238(n4112) mutation decreases mean lifespan by 20% [22482727]. | Nematode |
| mir-71 | — | Loss and gain-of-function of mir-71 decreases and increases lifespan, respectively [21129974]. mir-71 mutants have a reduced lifespan with 40% decrease in mean lifespan, while extra copies of mir-71 extend the lifespan with an increase in lifespan by 15 - 25% [22482727],
Loss of mir-71 function suppresses the long lifespan of glp-1(e2141) mutants [22482727],
During adulthood mir-71 is strongly expressed in the intestine, body wall muscles and neurons. mir-71 is upregulated in aging adults [22482727], | Nematode |
| lin-4 | abnormal cell LINeage 4 | A loss-of-function mutation in lin-4 shortens lifespan and accelerated tissue ageing while overexpressing lin-4 extends lifespan by redarding aging [16373574].
lin-4 is regulated by DAF-16 in L1 arrest. | Nematode |
| mir-14 | mir-14 stem loop | Mutating mir-14 decreases lifespan in both sexes. mir-14 reduces the mean and maximum lifespan of females by 55 and 36%, respectively, while those of males is reduced by 29 and 21%, respectively [12725740].
| Fruit fly |
| mir-34 | — | mir-34 loss triggers a gene expression profile of accelerated brain aging, late-onset brain degeneration and catastrophic decline in survival, while mir-34 upregulation extends median lifespan and mitigated neurodegeneration induced by polyglutamine. | Fruit fly |
| mir-277 | — | Constitutive miR-277 expression shortens lifespan and synthetically lethal with reduced insulin signaling, indicating that metabolic control underlies this phenotype. Transgenic inhibition with a miRNA sponge construct also shortens lifespan [23669073].
miR-277 is downregulated during adult life [23669073].
mir-277 controls branched-chain amino acid catabolism and as a result it can modulate the activity of TOR kinase [23669073]. | Fruit fly |
| MIR21 | MIRN21; hsa-mir-21; miR-21; miRNA21 | MIR21 is the most highly expressed microRNA gene in octogenarians and centenarians. MIR21 expression is higher under cardiovascular diseases and lower in centenarian offspring. MIR21 is correlated with C-reactive protein and fibrinogen levels. TGF-βR2 mRNA, a MIR21 target, exhibits the highest expression in leukocytes form a subset of octogenarians. MIR-21 may be a biomarker of inflammation [23041385]. | Human |
| MIR146B | microRNA 146b | miR-146a/b is significantly elevated during senescence as a compensatory response to restrain inflammation via the suppression of IL-6 and IL-8 secretion and downregulation of IRAK1 (component of IL-1 receptor signaling). Ectopic expression of miR-146a/b in primary fibroblasts suppresses IL-6 and IL-8 secretion and downregulation of IRAK1 [20148189]. | Human |
| MIR146A | microRNA 146a | miR-146a/b is significantly elevated during senescence as a compensatory response to restrain inflammation via the suppression of IL-6 and IL-8 secretion and downregulation of IRAK1 (component of IL-1 receptor signaling). Ectopic expression of miR-146a/b in primary fibroblasts suppresses IL-6 and IL-8 secretion and downregulation of IRAK1 [20148189]. | Human |
| MIR373 | microRNA 373 | miR-373 expression is able to bypass RAS-induced senescence in presence of wild-type p53 [16564011]. | Human |
| MIR372 | microRNA 372 | miR-372 expression is able to bypass RAS-induced senescence in presence of wild-type p53 [16564011]. | Human |
| MIR217 | microRNA 217 | MIR217 (alias hsa-miR-217) is significantly upregulated in senescent human mesenchymal stem cells (hMSCs) when compared to early passage hMSC, but overall had very low expression levels [18493317]. | Human |
| hsa-let-7f | — | hsa-let-7f is significantly upregulated in senescent human mesenchymal stem cells (hMSCs) when compared to early passage hMSC [18493317]. | Human |
| MIR499 | microRNA-449 | hsa-miR-499 is significantly upregulated in senescent human mesenchymal stem cells (hMSCs) when compared to early passage hMSC [18493317]. | Human |
| MIRC29 | microRNA 29c | hsa-miR-29c is significantly upregulated in senescent human mesenchymal stem cells (hMSCs) when compared to early passage hMSC [18493317]. | Human |
| MIR369 | microRNA 369 | hsa-miR-369-5p is significantly upregulated in senescent human mesenchymal stem cells (hMSCs) when compared to early passage hMSC [18493317]. | Human |
| MIR371A | microRNA 371a | hsa-miR-371 is significantly upregulated in senescent human mesenchymal stem cells (hMSCs) when compared to early passage hMSC [18493317]. | Human |
| MIR34C | microRNA 34c | — | Human |
| MIR34B | microRNA 34b | mir-34 family, particularly miR-34a, as downstream effectors of p53 involved in cell cycle [17656095], leads to cell cycle arrest, increased expression of Beta-galactosidase [17554337] and downregulation of E3F family target genes [17875987]. MDM2 inhibiting drug Nutlin-3, leads to p53 activation, induced up-regulation of primarily miR-34a and later miR-34b and miR-34c [18451145]. | Human |
| MIR34A | microRNA 34a | mir-34 family, particularly miR-34a, as downstream effectors of p53 involved in cell cycle [17656095], leads to cell cycle arrest, increased expression of Beta-galactosidase [17554337] and downregulation of E3F family target genes [17875987]. MDM2 inhibiting drug Nutlin-3, leads to p53 activation, induced up-regulation of primarily miR-34a and later miR-34b and miR-34c [18451145]. | Human |
| MIR29A | microRNA 29a | miR-29a reduces the amount of methylation and upregulates a long non-coding RNA form a region called MEG3 that is responsible for inducing apoptotic pathway. Thus reducing tumorgensis in non-malignant hepatocytes [21625215].
| Human |
