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Hallmarks of Aging: Difference between revisions
→The Hallmarks in Detail
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| style="background-color:hsla(180, 100%, 85%);" |'''DNA methylation shift''': DNA methylation is a biochemical process involving the addition of a methyl group to the DNA molecule, specifically to the cytosine or adenine DNA nucleotides. This process is a form of epigenetic modification, which means it can affect gene expression and function without changing the DNA sequence itself. | | style="background-color:hsla(180, 100%, 85%);" |'''DNA methylation shift''': DNA methylation is a biochemical process involving the addition of a methyl group to the DNA molecule, specifically to the cytosine or adenine DNA nucleotides. This process is a form of epigenetic modification, which means it can affect gene expression and function without changing the DNA sequence itself. | ||
|DNA methylation generally decreases with age in certain human and mouse tissues or cell cultures.{{pmid|3611071}}{{pmid|22689993}}{{pmid|35143257}}{{pmid|35501397}} The loss of methylation in CD4<sup>+</sup> T cells is proportional to age.{{pmid|22689993}} | |DNA methylation generally decreases with age in certain human and mouse tissues or cell cultures.{{pmid|3611071}}{{pmid|22689993}}{{pmid|35143257}}{{pmid|35501397}} The loss of methylation in CD4<sup>+</sup> T cells is proportional to age.{{pmid|22689993}} | ||
|No direct evidence yet | |No direct evidence yet. | ||
|No direct evidence yet | |No direct evidence yet. | ||
|Progeroid syndromes exhibit DNA methylation patterns similar to normal aging, suggesting a link with aging-related diseases{{pmid|20961378}}{{pmid|16738054}}. | |Progeroid syndromes exhibit DNA methylation patterns similar to normal aging, suggesting a link with aging-related diseases{{pmid|20961378}}{{pmid|16738054}}. | ||
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|Chronic expression of unfolded, misfolded or aggregated proteins contributes to the development of some age-related pathologies, such as Alzheimer’s disease, Parkinson’s disease and cataracts{{pmid|19298183}}. | |Chronic expression of unfolded, misfolded or aggregated proteins contributes to the development of some age-related pathologies, such as Alzheimer’s disease, Parkinson’s disease and cataracts{{pmid|19298183}}. | ||
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| style="text-align:center; background-color:hsla(210, 100%, 85%);" |'''Disabled | | style="text-align:center; background-color:hsla(210, 100%, 85%);" |'''Disabled macroautophagy'''[[File:Macro-micro-autophagy.gif|frameless|101x101px]] | ||
| style="background-color:hsla(210, 100%, 85%);" | | | style="background-color:hsla(210, 100%, 85%);" |'''Disabled macroautophagy''', often referred as impaired or dysfunctional autophagy, is a condition where the cellular process of autophagy—specifically the macroautophagy pathway—is disrupted or less effective. Autophagy is a critical cellular process for degrading and recycling damaged organelles, misfolded proteins, and other cellular debris. Macroautophagy involves the engulfment of these unwanted materials into vesicles called autophagosomes, which then fuse with lysosomes where the contents are degraded and recycled. When macroautophagy is disabled or impaired, cells accumulate damaged proteins and organelles, leading to cellular dysfunction and contributing to various diseases, particularly those related to aging and neurodegeneration. This loss of a crucial cellular "cleanup" mechanism can result in increased oxidative stress, disrupted cellular homeostasis, and an acceleration of the aging process. | ||
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| | While originally considered under hallmark '''altered proteostasis''', autophagy regulates a number of other hallmarks of ageing such as DNA repair and nutrient sensing/metabolism{{pmid|29626215}}, and hence it was proposed to be categorized as an integrative hallmark. | ||
|Compromised autophagy is observed in numerous ageing conditions including neurodegeneration and immunosenescence{{pmid|31144030}}{{pmid|34901876}}. | |||
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|Activation of autophagy can increase mouse lifespan{{pmid|29849149}}, and even improve immune response to vaccination in older humans by overcoming immunosenescence{{pmid|33317695}}. | |||
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