Hallmarks of Aging: Difference between revisions

Hallmarks of Aging (view source)

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 !Experimentally increasing it accelerates aging
 !Experimentally amending it slows the normal aging process and increases healthy lifespan.
+!Associated human diseases
 |-
 | style="text-align:center; background-color:hsla(180, 100%, 85%);" |[[File:DNA Structure+Key+Labelled.pn NoBB.png|frameless|76x76px]]
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 |Deficient DNA repair causes premature aging{{pmid|19812404}}
 |Increased DNA repair facilitates greater longevity{{pmid|19812404}}
+|
 |-
 | 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%);" |
+| style="background-color:hsla(180, 100%, 85%);" |Telomere attrition is a hallmark characterized by the progressive shortening of telomeres, due to the inability of DNA polymerases to fully replicate the ends of linear chromosomes. This shortening contributes to genomic instability, cellular aging, and limited cellular lifespan. Telomeres are protected by shelterin complexes; however, their deterioration or the absence of telomerase leads to cellular senescence and diseases.{{pmid|17024208}}{{pmid|18680434}}{{pmid|22426077}}{{pmid|22965356}}{{pmid|18252230}}{{pmid|18669893}}{{pmid|21205863}}{{pmid|20569239}}
-|
+|Telomere shortening is observed during normal aging in humans and mice{{pmid|17876321}}.
-|
+|Telomerase deficiency and severe uncapping of telomeres lead to premature aging and diseases{{pmid|22965356}}{{pmid|18680434}}{{pmid|18252230}}{{pmid|18669893}}{{pmid|21205863}}.
+|Extension of telomeres through telomerase reactivation or other means can delay aging and extend lifespan without increasing cancer risk{{pmid|21113150}}{{pmid|22585399}}{{pmid|21426483}}{{pmid|23346961}}.
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 | style="background-color:hsla(180, 100%, 85%);" |'''Epigenetic alterations'''
 | style="background-color:hsla(180, 100%, 85%);" |
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 | 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="background-color:hsla(0, 100%, 85%);" |'''Mitochondrial dysfunction'''
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 | style="background-color:hsla(30, 100%, 85%);" |[[Senescent Cells|'''Cellular senescence''']]
 | style="background-color:hsla(30, 100%, 85%);" |
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 | style="background-color:hsla(30, 100%, 85%);" |'''Stem cell exhaustion'''
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 '''(Microbiome disturbance)'''
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 '''(Inflammaging)'''
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 | style="background-color:hsla(30, 100%, 85%);" |'''Altered intercellular communication'''
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 |}
 ==History==