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| '''Genomic | | '''Genomic instability''' | ||
| Accumulation of DNA damage over time leading to cellular dysfunction. | | Accumulation of DNA damage over time leading to cellular dysfunction. | ||
| rowspan=" | | rowspan="6" |'''Primary Hallmarks''' | ||
(causes damage) | (causes damage) | ||
|- | |- | ||
| '''Telomere | | '''Telomere attrition''' | ||
| Reduction in the length of telomeres leading to cellular aging. | | Reduction in the length of telomeres leading to cellular aging. | ||
|- | |- | ||
| '''Epigenetic | | '''Epigenetic alterations''' | ||
| Changes in DNA methylation and histone modification affecting gene expression. | | Changes in DNA methylation and histone modification affecting gene expression. | ||
|- | |- | ||
| '''Loss of | |'''Splicing dysregulation''' | ||
|Impaired RNA construction from DNA, leading to cellular dysfunction. | |||
|- | |||
| '''Loss of proteostasis''' | |||
| Disruption in protein folding and stability leading to cell damage. | | Disruption in protein folding and stability leading to cell damage. | ||
|- | |- | ||
|'''Compromised | |'''Compromised autophagy''' | ||
|Impaired cellular maintenance through the consumption of own components. | |Impaired cellular maintenance through the consumption of own components. | ||
|- | |- | ||
|'''Deregulated | |'''Deregulated nutrient sensing''' | ||
| Alterations in nutrient sensing pathways affecting metabolism and aging. | | Alterations in nutrient sensing pathways affecting metabolism and aging. | ||
| rowspan="3" |'''Antagonistic Hallmarks''' | | rowspan="3" |'''Antagonistic Hallmarks''' | ||
(responses to damage) | (responses to damage) | ||
|- | |- | ||
|'''Mitochondrial | |'''Mitochondrial dysfunction''' | ||
| Decrease in mitochondrial efficiency and increase in oxidative stress. | | Decrease in mitochondrial efficiency and increase in oxidative stress. | ||
|- | |- | ||
|[[Senescent Cells|'''Cellular | |[[Senescent Cells|'''Cellular senescence''']] | ||
| Accumulation of non-dividing, dysfunctional cells secreting harmful factors. | | Accumulation of non-dividing, dysfunctional cells secreting harmful factors. | ||
|- | |- | ||
|'''Stem | |'''Stem cell exhaustion''' | ||
| Decline in the regenerative capacity of stem cells affecting tissue repair. | | Decline in the regenerative capacity of stem cells affecting tissue repair. | ||
| rowspan=" | | rowspan="5" |'''Integrative Hallmarks''' | ||
(culprits of the phenotype) | (culprits of the phenotype) | ||
|- | |- | ||
|'''Altered | |'''Altered intercellular communication''' | ||
| Changes in cellular communication leading to inflammation and tissue dysfunction. | | Changes in cellular communication leading to inflammation and tissue dysfunction. | ||
|- | |- | ||
|'''Microbiome disturbance (dysbiosis)''' | |||
|'''Microbiome | |||
|Changes in gut microbiome affecting health and aging. | |Changes in gut microbiome affecting health and aging. | ||
|- | |- | ||
|'''Inflammation (Inflammaging)''' | |'''Inflammation (Inflammaging)''' | ||
|Systemic inflammation contributing to aging and related diseases. | |Systemic inflammation contributing to aging and related diseases. | ||
|- | |||
|'''Altered mechanical properties''' | |||
|Changes in cellular and extracellular structure affecting tissue function. | |||
|} | |} | ||