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Hallmarks of Aging: Difference between revisions

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{| class="wikitable"
{| class="wikitable"
!
! Hallmark
! Hallmark
! Description
! Description
!
|-
|-
! rowspan="4" |Primary Hallmarks
| '''Genomic Instability'''
| Accumulation of DNA damage over time leading to cellular dysfunction.
| rowspan="4" |'''Primary Hallmarks'''
(causes damage)
(causes damage)
| Genomic Instability
| Accumulation of DNA damage over time leading to cellular dysfunction.
|-
|-
| Telomere Attrition
| '''Telomere Attrition'''
| Reduction in the length of telomeres leading to cellular aging.
| Reduction in the length of telomeres leading to cellular aging.
|-
|-
| Epigenetic Alterations
| '''Epigenetic Alterations'''
| Changes in DNA methylation and histone modification affecting gene expression.
| Changes in DNA methylation and histone modification affecting gene expression.
|-
|-
| Loss of Proteostasis
| '''Loss of Proteostasis'''
| Disruption in protein folding and stability leading to cell damage.
| Disruption in protein folding and stability leading to cell damage.
|-
|-
! rowspan="3" |Antagonistic Hallmarks
| '''Deregulated Nutrient Sensing'''
| Alterations in nutrient sensing pathways affecting metabolism and aging.
| rowspan="3" |'''Antagonistic Hallmarks'''
(responses to damage)
(responses to damage)
| Deregulated Nutrient Sensing
| Alterations in nutrient sensing pathways affecting metabolism and aging.
|-
|-
| Mitochondrial Dysfunction
| '''Mitochondrial Dysfunction'''
| Decrease in mitochondrial efficiency and increase in oxidative stress.
| Decrease in mitochondrial efficiency and increase in oxidative stress.
|-
|-
| [[Senescent Cells|Cellular Senescence]]
| [[Senescent Cells|'''Cellular Senescence''']]
| Accumulation of non-dividing, dysfunctional cells secreting harmful factors.
| Accumulation of non-dividing, dysfunctional cells secreting harmful factors.
|-
|-
! rowspan="2" |Integrative Hallmarks
| '''Stem Cell Exhaustion'''
| Decline in the regenerative capacity of stem cells affecting tissue repair.
| rowspan="2" |'''Integrative Hallmarks'''
(culprits of the phenotype)
(culprits of the phenotype)
| Stem Cell Exhaustion
| Decline in the regenerative capacity of stem cells affecting tissue repair.
|-
|-
| Altered Intercellular Communication
| '''Altered Intercellular Communication'''
| Changes in cellular communication leading to inflammation and tissue dysfunction.
| Changes in cellular communication leading to inflammation and tissue dysfunction.
|-
|-
! rowspan="5" |Proposed New Hallmarks
|'''Compromised Autophagy'''
|Compromised Autophagy
|Impaired cellular maintenance through the consumption of own components.
|Impaired cellular maintenance through the consumption of own components.
| rowspan="5" |'''Proposed New Hallmarks'''
|-
|-
|Splicing Dysregulation
|'''Splicing Dysregulation'''
|Impaired RNA construction from DNA, leading to cellular dysfunction.
|Impaired RNA construction from DNA, leading to cellular dysfunction.
|-
|-
|Microbiome Disturbance
|'''Microbiome Disturbance'''
|Changes in gut microbiome affecting health and aging.
|Changes in gut microbiome affecting health and aging.
|-
|-
|Altered Mechanical Properties
|'''Altered Mechanical Properties'''
|Changes in cellular and extracellular structure affecting tissue function.
|Changes in cellular and extracellular structure affecting tissue function.
|-
|-
|Inflammation (Inflammaging)
|'''Inflammation (Inflammaging)'''
|Systemic inflammation contributing to aging and related diseases.
|Systemic inflammation contributing to aging and related diseases.
|}
|}
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