|nhr-62 Mutation ||Mutation in *nhr-62* suppresses the lifespan extension of eat-2(ad465) animals (p<0.001) [Heestand et al. 2013]. ||Worm ||— ||— ||— |
|nhr-62 Overexpression ||Wild-type (N2) worms with extrachromosomal array dhEx627 (carrying a wild-type nhr-62) exhibit a significant increase in lifespan compared to wild-type (p<0.001) [Heestand et al. 2013]. ||Worm ||— ||— ||— |
|mrpl-37 RNAi ||Knockdown of mrpl-37 increases lifespan by 41% . ||Worm ||+41 ||— ||— |
|mrpl-2 RNAi ||Knockdown of mrpl-2 increases lifespan by 54% . ||Worm ||+54 ||— ||— |
|mrpl-1 RNAi ||Knockdown of mrpl-1 increases lifespan by 57% . ||Worm ||+57 ||— ||— |
|ttl-9 RNAi ||Knockdown of ttl-9 throughout the entire life increases the lifespan by 3% . ||Worm ||+3 ||— ||— |
|nkcc-1 RNAi ||Knockdown of nkcc-1 throughout the entire life increases the lifespan by 23% . ||Worm ||+23 ||— ||— |
|mrps-5 RNAi ||Knockdown of mrps-5 throughout the entire life increases the lifespan by 60%. mrps-5 RNAi prevents aging-associated functional decline and alters mitochondrial function. Knocking down mrps-5 after early development no longer affects nematode lifespan. When RNAi of mrps-5 was performed during the larval stages only, lifespan increases by 48%, whereas RNAi started from the L4 stage has no effect. mrps-5 RNAi results in fragmented mitochondria. mrps-5 RNAi increases lifespan by 40% in widltype, 37% in daf-16(mu86), 40% in sir-2.1(ok434) 69% in aak-2(ok524) and 112% in mev-1(kn1). Knockdown of cco-1 does not extend the lifespan of mrps-5 RNAi . ||Worm ||+60 ||— ||— |
|frh-1 RNAi ||Complete absence of frataxin is lethal, while its partial deficiency extends animal lifespan in a p53 dependent manner. Frataxin knockdown via RNAi extends mean and maximum lifespan by 19 and 37%, respectively .
Substantial reduction of frataxin protein expression is required to extend lifespan, affect sensory neurons functionality, remodel lipid metabolism and trigger autophagy. Beclin and p53 genes are required to induce autophagy and concurrently reduce lipid storages and extend animal lifespan in response to frataxin suppression . ||Worm ||+18.75 ||— ||+37.037037037 |
|Metformin treatment ||Metformin treatment extends healthspan, slows lipofuscin accumulation, extends mean lifespan and prolongs healthful locomotory ability in a dose-dependent manner as well as reduces fecundity. AMPK and its activating kinase LKB1 are essential for these health benefits. Oxidative stress-responsive transcription factor SKN-1/Nrf2 is essential for metformin-confered healthspan too as it must be expressed in both neurons and intestines . ||Worm ||— ||— ||— |
|wrn-1 mutation ||A nonfunctional wrn-1 DNA helicase decreases the lifespan .
The expression of miR-124 in whole wrn-1 mutant worms is significantly reduced .
Supplementation of vitamin C normalizes the median lifespan of wnr-1 and mir-124 mutants . ||Worm ||— ||— ||— |
|wrn-1 RNAi ||RNAi kockdown of wrn-1 shortens the lifespan, increases sensitivity to DNA damage, and accelerates aging phenoypes . ||Worm ||— ||— ||— |
|mir-124 mutation ||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 .
Supplementation of vitamin C normalizes the reduced median lifespan of mir-124 mutants . ||Worm ||— ||— ||— |
|mir-80 mir-227(nDf53); mir-81-82(nDf54) ||mir-80 mir-227(nDf53); mir-81-82(nDf54) mutation decreases the mean lifespan by 20% . ||Worm ||-20 ||— ||— |
|mir-64-66 mir-229(nDf63) mutation ||mir-64-66 mir-229(nDf63) mutation decreases the lifespan by 30% . ||Worm ||-30 ||— ||— |
|mir-61 mir-250(nDf59) mutation ||mir-61 mir-250(nDf59) mutation decreases the mean lifespan by 25% . ||Worm ||-25 ||— ||— |
|mir-58 mutation ||mir-58(n4640) mutation decreases the mean lifespan by 20% . ||Worm ||-20 ||— ||— |
|mir-14 mutation ||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 . ||Worm ||-29 to -55 ||— ||-21 to -29 |
|mir-239 mutation ||Mutating mir-239 increases mean and maximum lifespan by 12 and 36%, respectively. Lifespan extension by mir-239 loss-of-function requires daf-16 . ||Worm ||+11.8 ||— ||+36.0 |
|mir-239 overexpression ||Overexpressing mir-239 decreases mean and maximum lifespan by 13 and 17 - 33%, respectively . ||Worm ||-13 ||— ||-17 to -33 |
|mir-246 overexpression ||mir-246 overexpression increases mean and maximum lifespan by 6 and 5 - 14%, respectively . ||Worm ||+6.3 ||— ||+4.8 to +14.3 |
|mir-246 mutation ||Mutating mir-246 decreases mean and maximum lifespan by 12% . ||Worm ||-11.7 ||— ||-12.0 |
|mir-238 mutation ||Mutating mir-238 decreases mean and maximum lifespan by 18 and 24% . mir-238(n4112) mutation decreases mean lifespan by 20% . ||Worm ||-17.6 to -20 ||— ||-24 |
|mir-71 overexpression ||Gain-of-function of mir-71 increases lifespan . Extra copies of mir-71 extend the lifespan with an increase in lifespan by 15 - 25% , ||Worm ||+15 to +25 ||— ||— |
|lin-14 RNAi ||Knockdown of lin-14 only during adulthood is sufficient to extend lifespan and suppresses the short lifespan phenotype of lin-4 mutants. ||Worm ||— ||— ||— |