Denigma

Datasets

Changes

Denigma cartographies changes from the molecular level to whole physiology which occur in defined contrasts such as aging and dietary as well as genetic lifespan-extending interventions:

  • aging (young vs. old)
  • dietary (DR vs. AL)
  • genetic (mutant vs. wild-type) o
ID name taxid reference pmid tissue comparision start stop gender description
26 Trimethylamine decreases 10090 Wijeyesekera et al., 2012 22225495 Plasma Diet 30% DR for 48h at 16 weeks — male —
27 Trimethylamine decreases 10090 Wijeyesekera et al., 2012 22225495 Plasma Mutant Irs1-/- at 16 weeks — male —
28 Trimethylamine decreases 10090 Wijeyesekera et al., 2012 22225495 Plasma Mutant Irs1df/df at 16 weeks — male —
29 Choline decreases 10090 Wijeyesekera et al., 2012 22225495 Plasma Diet 30% DR for 48h at 16 weeks — male —
30 Glycerophosphocholine decreases 10090 Wijeyesekera et al., 2012 22225495 Plasma Diet 30% DR for 48h at 16 weeks — male —
31 Glycerophosphocholine decreases 10090 Wijeyesekera et al., 2012 22225495 Plasma Mutant Irs1-/- at 16 weeks — male —
32 Glycerophosphocholine increases 10090 Wijeyesekera et al., 2012 22225495 Plasma Mutant Irs1df/df at 16 weeks — male —
33 Trimethylamine-N-Oxide increases 10090 Wijeyesekera et al., 2012 22225495 Plasma Diet 30% DR for 48h at 16 weeks — male —
34 Scyllo-inositol increases 10090 Wijeyesekera et al., 2012 22225495 Plasma Mutant Irs1-/- at 16 weeks — male —
36 alpha- and beta-glucose decreases 10090 Wijeyesekera et al., 2012 22225495 Plasma Diet 30% DR for 48h at 16 weeks — male —
37 Glycine decreases 10090 Wijeyesekera et al., 2012 22225495 Plasma Diet 30% DR for 48h at 16 weeks — male —
38 HDL increases 9606 Fontana et al., 2004 15096581 Plasma Diet Chronic DR — — —
46 DHEA declines 9606 Jeff — — — 70 — male —
48 Growth hormone declines 9606 — — — Age 70/35 year — male/female —
49 Progesterone declines 9606 — — — Age 70/35 year — male/female —
75 Metabolic and mitochondrial decline 10090 — 22585399 — age — — males/females 2 years old mice exhibit metabolic and mitochondrial decline [22585399].
84 Cell proliferation increases 1016 11744049 — — Diet — — — 24 month DR in rats enhances cell proliferation in duodenum and forestomach mucosal tissue [11744049].
85 Cell proliferation decreases 10116 — 11744049 — Diet — — — 24 month DR in rats inhibits cell proliferation in glandular stomach and liver tissue [11744049].
70 IGF1 levels decline 9606 — 3322823 plasma age — — — A decline in IGF1 expression occurs with age progression. Levels of circulating IGF1 in humans are low at birth, rise progressively during childhood and peak during midadolescence, and then progressively fall as a function of age. Reduction in levels of circulating IGR1 is related to decreased secretion of growth hormone [3322823].
64 Decrease in WNT gene expression 9606 RoSyBa 2011 — adipose-derived stem cells age 40 year 60 year females A dramtic decrease in WNT gene expression occurs in Adipose-dreived stem cells from females at the age of 40-60 years [RoSyBa 2011].
40 Accumulation of lipofuscin-like fluorescent pigment 6239 Apfeld et al., 2004 15574588 intestine Age 1 day 7 day Hemaphrodite A lipofuscin-like fluorescent pigment accumulates in an age-dependent manner in the intestine (Garigan et al., 2002; Herndon et al., 2002). It accumulates at a faster rate in aak-2 mutant, which have a shortened lifespan [15574588].
88 Structural chromosome variation 9606 — — — — — — — Acquired differences in structural chromosome variants between members of monozygoutic twin pairs (including mosaic anomalis) are observed in pairs of >55 years of age but not in younger [29 in Laurie et al. 2012].
103 Decreased stem cell activity — — 20504968 — age — — — Advanced age is associated with decreased stem cell activity [20504968].
131 Arterial walls stiffen with age — López-Andrés et al. 2012 23172930 — — — — — Age-associated changes in blood vessels include the increase in inflammatory response, cell loss, inability to repair DNA damage, oncogene activation and regulation of telomere-telomerase complex [9-11]. Several age-associated structural, functional, and molecular changes occur in the arterial system. Aging is accompanied with thickening and dilatation of large arteries, extracellular matrix accumulation, calcium deposits, increased vascular stiffness, and endothelial dysfunction [12,13]. These alterations may be attributable to age-related functional changes in vascular cells [12]. Age-related arterial inflammatory phenotype includes increased expression of monocyte chemoattractant protein 1, intercellular adhesion molecule 1, matrix metalloproteinase-2 activity, or transforming growth factor-β expression [14,15]. Age-associated changes in blood vessels include a decrease in compliance, and increase in arterial stiffness and arterial wall thickening as a result of increased vascular calcifications, increased collagen content and cross-linking, and decreased elastin content [16,18]. References =========== 9. Lakatta EG. Cardiovascular regulatory mechanisms in advanced age. Physiol Rev. 1993;73:413–467. 10. Serrano M, Blasco MA. Putting the stress on senescence. Curr Opin Cell Biol. 2001;13:748–753. 11. Wei JY. Age and the cardiovascular system. N Engl J Med. 1992;327:1735–1739. 12. Lakatta EG. Arterial and cardiac aging: major shareholders in cardiovascular disease enterprises: Part III: cellular and molecular clues to heart and arterial aging. Circulation. 2003;107:490–497. 13. Lakatta EG, Wang M, Najjar SS. Arterial aging and subclinical arterial disease are fundamentally intertwined at macroscopic and molecular levels. Med Clin North Am. 2009;93:583–604, Table of Contents. 14. Spinetti G, Wang M, Monticone R, Zhang J, Zhao D, Lakatta EG. Rat aortic MCP-1 and its receptor CCR2 increase with age and alter vascular smooth muscle cell function. Arterioscler Thromb Vasc Biol. 2004;24:1397–1402. 15. Wang M, Zhao D, Spinetti G, Zhang J, Jiang LQ, Pintus G, Monticone R, Lakatta EG. Matrix metalloproteinase 2 activation of transforming growth factor-beta1 (TGF-beta1) and TGF-beta1-type II receptor signaling within the aged arterial wall. Arterioscler Thromb Vasc Biol. 2006;26:1503–1509. 16. Lacolley P, Labat C, Pujol A, Delcayre C, Benetos A, Safar M. Increased carotid wall elastic modulus and fibronectin in aldosterone-salt-treated rats: effects of eplerenone. Circulation. 2002;106:2848–2853. 17. López-Andrés N, Martin-Fernandez B, Rossignol P, Zannad F, Lahera V, Fortuno MA, Cachofeiro V, Díez J. A role for cardiotrophin-1 in myocardial remodeling induced by aldosterone. Am J Physiol Heart Circ Physiol. 2011;301:H2372–H2382. 18. Zieman SJ, Melenovsky V, Kass DA. Mechanisms, pathophysiology, and therapy of arterial stiffness. Arterioscler Thromb Vasc Biol.2005;25:932–943.
59 Deteriorarition of circadian rhytms 10090 Farajnia, et al 2012 — Suprachiasmatic Nucleus age 2 month 30 month — Aged mice have disrupted sleep hevaiour and weakened brain network activity in the SCN. Aged SCN neurons lack day-night rhythms in some membrane properties. There is an age-related reductions of certain potassium currents that are import to the neuron’s rhythmic firing. Behavioral and sleep-wake rhythms exhibit a strong fragmentation, starting at the age of 700 d. Aged mice are deficient in membrane properties and GABAergic postsynaptic current amplitude. Aging mice selectively loss circadian modulation of fast-delayed-rectifer and A-type K+ currents. In aged mice at the tissue level, the phase synchrony of SCN neurons was grossly disturbed, with some subpopulations peaking in anti-phase and a reduction in amplitude of the overall multiunit activity rhythm.

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