| Cold temperature | A reduction of the environmental temperature form 25 to 18 degree Celsius increases mean and maximum lifespan by 108 and 62% in Canton-S male [8582611]. | Fly | +108 | — | +62 |
| ATP2 Mutation | A temperature sensitive allele of ATP2 causes a clonal senescence phenotype resulting from the disruption of the age asymmetry between mother and daughter cells in that that daughter cells are born as old as they mother cells at 36 degree Celsius. This Mutation of valine to isoleucine at amino acid 90 does not affect growth on non-fermentable carbon source. This allele is associated with loss of mitochondrial membrane potential as well as failure to segregate functional mitochondria to daughter cells [12242224]. | Worm | — | — | — |
| aak-1 mutation | aak-1 does not appear to be required for the control of lifespan [15574588]. | Worm | — | — | — |
| aak-2 mutation | aak-2(ok524) knockout mutants have a 12% and 18% shorter mean and maximum lifespan, respectively as well as faster age-dependent accumulation of a lipofuscin-like fluorescent pigment in the intestine [15574588]. aak-2 mutation suppresses lifespan extension and delay of the decline in locomotor activity resulting from sDR [17900900]. aak-2 mutation cancels out the lifespan extension effect of sDR and PD, regardless of the concentration of bacteria or peptones. bDR significantly extends lifespan of aak-2 mutants, but to lesser extent than that of wild-type. eat-2 mutation extends the lifespan of aak-2 mutants to the same extent than that of wild-type. Resveratrol does not increase lifespan of aak-2 mutants [19239417]. daf-2(m577);aak-2(ok524) double mutant has a lifespan that is indistinguishable from those of aak-2(ok524) single mutant [15574588]. | Worm | -12 | — | -18 |
| abce-1 RNAi | abce-1 RNAi in the adulthood extends the lifespan [New longevity regulators]. | Worm | — | — | — |
| abi-1 RNAi | abi-1 RNAi in the adulthood extends the lifespan [New longevity regulators]. | Worm | — | — | — |
| Germ-cell precursor ablation | Ablation of the germ-cell precursor, Z2 and Z3 as well as the precursors of the somatic gonad, Z1 and Z4 does not affect lifespan [8247153]. | Worm | — | — | — |
| ABP1 deletion | ABP1 deletion increases replicative lifespan by 30% in the alpha strain and decreases replicative lifespan by 20% in the a strain [18340043]. Deletion of ABP1 increases replicative lifespan by 20% in the alpha strain and decreases replicative lifespan by 20% in the a strain [19030232]. | Yeast | -20 to +30 | — | — |
| Ctf1 knockout | Absence of Ctf1 is associated with decreased arterial fibrosis, stiffness mad senescence and increased longevity. Ctf1-null mice have a decrease in arterial stiffness and decrease in levels of inflammatory, apoptotic and senescence, whereas telomere-linked and DNA repair proteins as well as antioxidant enzyme activities are increased. The median lifespan of Ctf1-null mice is increased by 5 month (18%) [23172930].
Wild-type and Ctf1-null mice exhibit an increase of senescence markers (p53, Mdm2, p21, and p16) with age but are lower in Ctf1-null mice. Ctf1-null mice have a diminished vascular NFκB signaling, lower inflammation and oxidative stress and reduced senescence. Ctf1-null mice have a 12% increase in body weight, 130% increased adiponectin levels and 51% decreased leptin concentrations [23172930]. | Mouse | — | +18 | — |
| Nlaz mutation | Absence of Nlaz, which is homologous to ApoD, results in a reduced lifespan in both sexes. Median lifespan is 30.8% and 22.5% lower in females and males, respectively. Maximum lifespan is reduced by 12% and 30% in females and males [21376794]. | Fly | — | -22.5 to -30.8 | -12 to -30 |
| TEC1 deletion | Absence of TEC1 causes a significant shortened chronological lifespan, but does not block chronological lifespan extension by rapamycin [21840851]. | Yeast | — | — | — |
| Ilp5 mutation | Abundance of Ilp5 mRNA is reduced under DR. Ilp5 null mutants have a normal lifespan under AL and a normal DR response. Ilp2 Ilp3 Ilp5 triple null mutants fail to have a normal response to DR. Their response is right shifted, with mutants being shorter-lived compared to wild-type on low but longer-lived on high yeast concentrations [20195512]. | Fly | — | — | — |
| Acacb knockout | Acacb-null animals (alias Acc2-/-) exhibit upon regular diet an increase triglyceride breakdown, leaner phenotype, increased insulin sensitivity and no effect on lifespan [17923673]. | Mouse | — | — | — |
| ACB1 deletion | ACB1 deletion extends chronological lifespan under starvation/extreme DR. Similar heat-shock resistance and resistance to a very hight concentration of acetic acid (but not resistance to oxidative stress) was enhanced by the deletion of ACB1. Deletion of ACB1 in W303-1A and DBY746 genetic backgrounds on synthetic complete media causes severe growth defects and sightly shorter lifespan and also heat-sensitivity [20657825]. | Yeast | — | — | — |
| ACH1 deletion | ACH1 deletion cells accumulate a high amount of extracellular acetic acid and display a reduced mean and maximum chronological lifespan. Maximum lifespan is reduced by 32%. Lifespan shortening is completely abrogated by alleviating the acid stress either by a DR regimen that prevents acetic acid production or by transferring chronologically aging mutant cells to water. Deletion of ACH1 is accompanied by reactive oxygen species accumulation, severe mitochondrial damage, and an early insurgence of apoptosis [22754872]. | Yeast | — | — | -32 |
| Deletion of mitochondrial DNA | Activation of the retrograde response by deletion of mitchondrial DNA (rho0) extends mean and maximum replicative lifespan by 24 - 51% and 15 - 65%, respectively [10224252]. Lifespan extension associated with impaired mitochondria depends on a retrograde intracellular signalling involving at leas three transcription factors, which adjust nuclear gene expression an induce shift of metabolism from Krebs cycle to the glyoxylate cycle [Refs 41,42 i Lee et al., 2002]. | Yeast | +24 to +51 | — | +15 to +65 |
| Adcy5 knockout | Adcy5 knockout mice are to cardiac stress and have an increased median lifespan of 30% as well as an increased maximal lifespan of 12%. Further, they are also protected from age-related reduced bone density and susceptibility to fractures, and reduced cardiac function [17662940]. | Mouse | — | +30 | +12 |
| D-glucosamine treatment | Addition of 0.5 mg/ml D-glucosamine to the growth media suppresses the short replicative lifespan and temperature sensitive growth of mpt5 mutant, but fails to extend the lifespan of wild-type cells [11805047]. | Yeast | — | — | — |
| (R)-N-(2-heptyl)-N-methylpropargylamine treatment | Addition of 0.66 ng/fly/day (R)-N-(2-heptyl)-N-methylpropargylamine to a sucrose-based diet resulted in no significant effect on lifespan, but lifespan reduction due to galactose feeding is partially suppressed by supplementation with (R)-deprenyl or (R)-N-(2-heptyl)-N-methylpropargylamine [9972869]. | Fly | — | — | — |
| 2-MEA treatment | Addition of 1% by weight 2-MEA to the diet of male LAF mice, started shortly after weaning, increases average lifespan by approximately 30%, but does not extend maximum lifespan [5723482; 11795501].
Addition of 2-MEA to the maternal diet of female mice increases the lifespan of male and female offspring by 15 and 8%, respectively [Harman & Eddy, 1979; 11795501].
Addition of 2-MEA of an antioxidant mixture containing ethoxyquin and 2-MEA to the diet of dietary restricted mice shortens lifespan approximately 20% [2394907]. | Mouse | +30 | — | — |
| ADE4 deletion | ade4 mutation extends chronological lifespan, but not replicative lifespan, and is non-additive with 0.5% glucose or amino-acid DR on chronological lifespan extension. ADE4 deletion in atg16 mutants results only in a partial extension of the chronological lifespan by 0.5% glucose DR [20421943]. | Yeast | — | — | — |
| Carboxyfullerene SOD mimetic treatment | Administration of a small-molecule synthetic enzyme superoxide dismutase mimetic to wild-type (i.e. non-transgenicm non-senescence accelerated) mice starting at middle age significantly extends lifespan and reduces age-associated oxidative stress and mitochondrial radical production. Treatment also improves performance on Morris water maze learning and memory task and therefore rescues age-related cognitive impairment [17079053]. | — | — | — | — |
| Spermidine | Administration of spermidine extends lifespan of yeast, flies and worms and human immune cells. In yeast spermidine treatment triggers deacetylation of H3 through inhibition of histone acetylatranserfases, suppresses oxidative stress and necrosis. Altered acetylation of the chromatin results in upregulation of various autophagy-related genes and triggers autophagy [19801973]. | — | — | — | — |
| Phloridzin treatment | Administration of the apple polyphenol phloridzin at doses of 3, 10, and 30 microMolar siginificantly prolongs the replicative lifespan in K6001 strain (p < 0.01; p < 0.001). Phloridizin improves the viability of cells under oxidative stress (7 microMolar H2O2) in a dose-dependent manner and increases the significantly the expression of SOD1, SOD2, and SIR2 [21597195]. | Worm | — | — | — |
| alg-1 RNAi | Adult-specific knockdown of the C. elegans argonaute-like gene 1 *alg-1* results in shortened lifespan with a reduction in the mean and maximum lifespan by 9 - 16% and 14%, respectively [21810936]. | Worm | -9.6 to -16.1 | — | -13.7 |
GenAge
GenDR
