We need to know every factor which determines lifespan.

Lifespan factors often but not always originate from defined genetic elements. They are not just genes, by definition they can be anything for which a Classifications schema can be build for that is related to the regulation of lifespan, such entities may include Single-Nucleotide Polymorphism, transcript variants, proteins and their complexes, compounds (i.e. small molecules like metabolites and drugs), etc. A factor should be based on a defined molecular entity or genomic position and been classified. It shall be highly flexible and scalable Concept.

While individual lifespan factors within each species or precise defined molecular entities will be captured within the Lifespan App, Data Entries of the Data App may summarize for instance the relevance of each factor class (e.g. homologous group; chemical derivate of related structure and properties, etc.) as well as draw overall conclusions. o


  • symbol name observation species
    Interleukin 6 IL-6 House mouse
    Gdf11 growth differentiation factor 11 GDF11 is a circulating factor in young mice that declines with age. Treatment of old mice to restore GDF11 to youthful levels recapitulated the of young-old parabiosis and reverses age-related hypertrophy. House mouse
    Nudt1 nudix (nucleoside diphosphate linked moiety X)-type motif 1 hMTH1-Tg mice express high levels of the hMTH1 hydrolase that degrades 8-oxoGTP and 8-oxoGTP and excludess 8-oxoguanine from both DNA and RNA. hMTH1-overexpresing mice have significantly lower steady-state levels of 8-oxoguanine in both nuclear and mitochondrial DNA of several organs, including the brain. hMTH1 overexpression prevents the age-dependent accumulation of DNA 8-oxoguanine that occurs in the wild-type mice. These lower levels of oxidized guanines are associated with increased longevity and hMTH1-Tg animals live significantly longer than their wild-type littermates [23648059]. House mouse
    Mir669c microRNA 669c Expression increases with age in mouse liver. The miRNA downregulates detoxification and regeneration genes, which may contribute to aging [18561983]. House mouse
    miR-214 microRNA 214 Expression increases with age in mouse liver. The miRNA downregulates detoxification and regeneration genes, which may contribute to aging [18561983]. House mouse
    Mir27a MicroRNA 27a In Ames dwarf mice (which displays delayed Aging), Mir27a expression is significantly higher than in control mice. Mir27a may be responsible for delayed Aging in dwarf mice: it suppresses the expression of ODC1 and SRM, which in turn suppresses polyamine synthesis in dwarf mice liver. Part of the ability of dwarf mice to suppress or avoid tumor or Cancer growth may be attributed to the decreased Polyamine biosynthesis. [19878148] House mouse
    Mir489 microRNA 489 Mir489 is maintaining adult stem cells in quiescence phase. Inhibition of miR489 is sufficient to make murine satellite muscle cells exit the quiescence phase and enter the cell cycle through downregulation of the oncogene Dek [22358842]. House mouse
    Mir133 miR-133 is associated with stem cell differentiation in mouse and human ESCs [18371447]. House mouse
    Mir1 miR-1 is associated with stem cell differentiation in mouse and human ESCs [18371447]. House mouse
    Srf Serum Response Factor SRF is activated by the daily variations of a blood signal, resulting in significant changes in the structure and size of live cells throughout the course of the day [23374345]. Daily variations of plasma signal cyclically stimulates SRF. SRF is solicited in an antiphasic manner in humans and rats, a fact that is linked to their activity, diurnal and nocturnal, respectively. SRF activation is accompanied by a remodeling of the cellular "skeleton", resulting in morphological change in cells based on their activity [23374345]. House mouse
    Drd4 Dopamine D4 Receptor Drd4 knockout mice, when compared with wild-type and heterozygous mice, display a 7 - 9.7% decrease in lifespan, reduced spontaneous locomotor activity, and no lifespan increase when reared in an enriched environment [23283341]. House mouse
    2-MEA 2-Mercaptoethylanime hydrochloride 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]. References ---------------- Harman, D., and Eddy, D. E. (1979). Free radical theory of aging: beneficial effect of adding antioxidants to the maternal mouse diet on life span of offspring: possible explanation of the sex difference in longevity. Age 2, 109-22. House mouse
    2-ME 2-Mercaptoethanol Animals fed a diet supplemented with 2-mercaptoethanol (2-ME) exhibit an increased mean and maximum lifespan [6334792]. T-cell-dependent immune responses are higher in the 2-ME-fed mice compared to the controls when the animals are young. The accumulation of fluorescent products of lipid peroxidation damage is also delayed in the lymphocytes of the 2-ME-fed mice and tumor onset and incidence is reduced in these animals [6334792]. House mouse
    CCL2 chemokine (C-C motif) ligand 2 CCL2 levels are evaluated in old unpaired and young heterochronic (with old animals) paired mice [21886162]. House mouse
    CCL11 chemokine (C-C motif) ligand 11 CCL11 is an age-related systemic factor associated with decreased neurogenesis. Relative levels of CCL11 increase in the plasma during aging an in young mice during Heterochronic Parabiosis [21886162]. House mouse
    alpha-LA Lipoic Acid In rats, LA confers a memory effect, by fixing the lifespan of previous feeding regimen. When animals are switched early in life (12 months) from DR to AL and supplemented with α-lipoic acid the DR typical lifespan extension is maintained, but switching early from AL supplemented with α-lipoic acid to DR blocks the lifespan extending effect [18486188]. LA exhibits the ability to compensate for age-related, long-term memory deficits in old rats [8309958] and improves the memory and learning in progeriod mice [15627516]. Culturing LA, protects neurons against death induced by hyperoxia, glutamate, iron and H2O2 [12087131; 11602326]. House mouse
    Vegf Vascular endothelial growth factor A Vegf exhibits rhythmic expression in the liver [17360649]. Vegf expression is affected by the circadian organization of molecular clockwork. Levels of Vegf mRNA fluctuate in a circadian fashion. Period2 and Cryptochrome inhibit the Vegf promoter [14612524]. House mouse
    Prkaa1 Protein kinase, AMP-activated, alpha 1 catalytic subunit Prkaa1 hosphorylates Cryptochromes and leads to their degradation [19833968]. House mouse
    Klf10 Kruppel-like factor 10 Klf10 is circadian, induced by glucose, binds and represses Arntl promoter. Klf10 RNAi caused cellular period shortening (of Arntl- and Per2-luc) [20070857]. House mouse
    Rgs16 Regulator of G-protein signaling 16 Rgs16 knockdown have shorter free-running period of locomotors activity rhythm and reduced total activity. Under daytime RF food-anticipatory activity is attenuated and phase-advance of rhythmic Per2 expression in liver and thalamus is diminished [21408016]. House mouse
    Gnas GNAS (guanine nucleotide binding protein, alpha stimulating) complex locus Mutants in which the Gnasxl transcript is deleted from the Gnas gene, have a high metabolism and are very lean despite consuming more food. The mutant appears to have fewer glial cells in the suprachiasmatic nucleus where the circadian clock is controlled [22253771]. House mouse
    Diabenol In female NMRI and transgenic HER-2/neu mice supplementation of diabenol with drinking water 5 times a week since the age of 2 months, increases survival and inhibits spontaneous carcinogenesis. In NMRI diabenol does not influence body weight gain dynamics, food and water consumption, but slowed down age-related disturbances in estrous function and increases the lifespan of all and 10% most long-living ones. Diabenol treatment in NMRI mice also inhibits spontaneous tumor incidence (mammary and lymphomas mainly) and increases mammary tumor latency. Diabenol treatment slows down age-related changes in estrous function in HER-2/neu mice, but fails to influence survival and slightly inhibited the incidence and decrease the size of mammary adenocarcinoma metastasis into the lung [15754958]. House mouse
    Wrn Mice lacking the helicase domain of the WRN ortholog exhibit many phenotypic features of Werner Syndrom, including a pro-oxidant status and a shorter mean lifespan. Mice with a deletion in the helicase domain [9789047] recapitulates most of the Werner syndrome phenotypes, including an abnormal hyaluronic acid excretion, higher reactive oxygen species levels, dyslipidemia, increased genomic instability, and cancer incidence. Wrn(Dehl/Dehl) mutant mice have a 10 - 15% decrease in their mean lifespan [12707040; 19741171]. House mouse
    Igf2 insulin-like growth factor 2 Altered imprinting of Igf2 does not affect longevity [20550518]. House mouse
    Ctf1 Cardiotrophin 1 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]. Treatment of cells with CT-1 increases SA-β-galactosidase, and apotosis and senescence makers (p53, p21 and p16), without modifying Mdm2 expression [23172930]. House mouse
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    • 25 of 113 factors
    Factors are an extension of GenAge and GenDR.

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