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Hallmarks of Aging: Difference between revisions
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== The Hallmarks in Detail == | == The Hallmarks in Detail == | ||
{| class="wikitable" | |||
! colspan="2" |Hallmark | |||
! Background | |||
!Manifesting | |||
!Increasing | |||
!Amending | |||
|- | |||
| style="text-align:center; background-color:hsla(180, 100%, 85%);" |[[File:DNA Structure+Key+Labelled.pn NoBB.png|frameless|76x76px]] | |||
| style="background-color:hsla(180, 100%, 85%);" |'''Genomic instability''' | |||
| style="background-color:hsla(180, 100%, 85%);" |Damange in the DNA are formed mainly through oxidative stress and environmental factors.<ref>{{Cite journal|last=De Bont|first=R.|date=2004-05-01|title=Endogenous DNA damage in humans: a review of quantitative data|journal=Mutagenesis|language=en|volume=19|issue=3|pages=169–185|doi=10.1093/mutage/geh025|pmid=15123782|issn=1464-3804|doi-access=free}}</ref> A number of molecular processes work continuously to repair this damage.<ref>{{Cite journal|last=de Duve|first=Christian|date=2005-02-09|title=The onset of selection|journal=Nature|volume=433|issue=7026|pages=581–582|doi=10.1038/433581a|pmid=15703726|bibcode=2005Natur.433..581D|s2cid=4355530|issn=0028-0836|doi-access=free}}</ref> | |||
|DNA damage accumulates over time<ref name=":1">{{Cite journal|last1=Vijg|first1=Jan|last2=Suh|first2=Yousin|date=2013-02-10|title=Genome Instability and Aging|url=http://www.annualreviews.org/doi/10.1146/annurev-physiol-030212-183715|journal=Annual Review of Physiology|language=en|volume=75|issue=1|pages=645–668|doi=10.1146/annurev-physiol-030212-183715|pmid=23398157|issn=0066-4278}}</ref> | |||
|Deficient DNA repair causes premature aging<ref name=":0">{{Cite journal|last=Hoeijmakers|first=Jan H.J.|date=2009-10-08|title=DNA Damage, Aging, and Cancer|url=http://www.nejm.org/doi/abs/10.1056/NEJMra0804615|journal=New England Journal of Medicine|language=en|volume=361|issue=15|pages=1475–1485|doi=10.1056/NEJMra0804615|pmid=19812404|issn=0028-4793}}</ref> | |||
|Increased DNA repair facilitates greater longevity<ref name=":0" /> | |||
|- | |||
| style="text-align:center; background-color:hsla(180, 100%, 85%);" |[[File:Telomeres transparent.png|frameless|88x88px]] | |||
| style="background-color:hsla(180, 100%, 85%);" |'''Telomere attrition''' | |||
| style="background-color:hsla(180, 100%, 85%);" | | |||
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| style="text-align:center; background-color:hsla(180, 100%, 85%);" |[[File:Epigenome-transparent-upscale.png|frameless|85x85px]] | |||
| style="background-color:hsla(180, 100%, 85%);" |'''Epigenetic alterations''' | |||
| style="background-color:hsla(180, 100%, 85%);" | | |||
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| style="text-align:center; background-color:hsla(210, 100%, 85%);" |[[File:Stress signaling.png|frameless|95x95px]] | |||
| style="background-color:hsla(210, 100%, 85%);" |'''Loss of proteostasis''' | |||
| style="background-color:hsla(210, 100%, 85%);" | | |||
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| style="text-align:center; background-color:hsla(210, 100%, 85%);" |[[File:Macro-micro-autophagy.gif|frameless|101x101px]] | |||
| style="background-color:hsla(210, 100%, 85%);" |'''Disabled autophagy''' | |||
| style="background-color:hsla(210, 100%, 85%);" | | |||
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| style="text-align:center; background-color:hsla(0, 100%, 85%);" |[[File:Aiga restaurant knife-fork crossed.png|frameless|75x75px]] | |||
| style="background-color:hsla(0, 100%, 85%);" |'''Deregulated nutrient sensing''' | |||
| style="background-color:hsla(0, 100%, 85%);" | | |||
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|- | |||
| style="text-align:center; background-color:hsla(0, 100%, 85%);" |[[File:Mitochondrion mini.svg|frameless|92x92px]] | |||
| style="background-color:hsla(0, 100%, 85%);" |'''Mitochondrial dysfunction''' | |||
| style="background-color:hsla(0, 100%, 85%);" | | |||
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| style="text-align:center; background-color:hsla(30, 100%, 85%);" |[[File:DALL·E 2023-10-15 05.28.43 - Photo of senescent cells magnified under a microscope, showing their characteristic enlarged and flattened morphology. The cells are stained with a bl.png|frameless|75x75px]] | |||
| style="background-color:hsla(30, 100%, 85%);" |[[Senescent Cells|'''Cellular senescence''']] | |||
| style="background-color:hsla(30, 100%, 85%);" | | |||
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| style="text-align:center; background-color:hsla(30, 100%, 85%);" |[[File:Stem cell differentiation.svg|frameless|106x106px]] | |||
| style="background-color:hsla(30, 100%, 85%);" |'''Stem cell exhaustion''' | |||
| style="background-color:hsla(30, 100%, 85%);" | | |||
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| style="text-align:center; background-color:hsla(30, 100%, 85%);" |[[File:202004 Gut microbiota.svg|frameless|75x75px]] | |||
| style="background-color:hsla(30, 100%, 85%);" |'''Dysbiosis''' | |||
'''(Microbiome disturbance)''' | |||
| style="background-color:hsla(30, 100%, 85%);" | | |||
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| style="text-align:center; background-color:hsla(30, 100%, 85%);" |[[File:Histopathology of acute and chronic inflammation of the gastro-esophageal junction, annotated.jpg|frameless|75x75px]] | |||
| style="background-color:hsla(30, 100%, 85%);" |'''Chronic inflammation''' | |||
'''(Inflammaging)''' | |||
| style="background-color:hsla(30, 100%, 85%);" | | |||
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| style="text-align:center; background-color:hsla(30, 100%, 85%);" |[[File:Forms of Cell Signaling.png|frameless|75x75px]] | |||
| style="background-color:hsla(30, 100%, 85%);" |'''Altered intercellular communication''' | |||
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==History== | ==History== | ||