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Hallmarks of Aging: Difference between revisions

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!Associated human diseases
!Associated human diseases
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| style="text-align:center; background-color:hsla(180, 100%, 85%);" |'''Genomic instability'''[[File:DNA Structure+Key+Labelled.pn NoBB.png|frameless|76x76px]]
| style="text-align:center; background-color:hsla(180, 100%, 85%);" |'''[[Genomic Instability|Genomic instability]]'''[[File:DNA Structure+Key+Labelled.pn NoBB.png|frameless|76x76px]]
| style="background-color:hsla(180, 100%, 85%);" |Damange in the DNA are formed mainly through oxidative stress and environmental factors.{{pmid|15123782}} A number of molecular processes work continuously to repair this damage.{{pmid|15703726}}
| style="background-color:hsla(180, 100%, 85%);" |Damange in the DNA are formed mainly through oxidative stress and environmental factors.{{pmid|15123782}} A number of molecular processes work continuously to repair this damage.{{pmid|15703726}}
|DNA damage accumulates over time{{pmid|23398157}}
|DNA damage accumulates over time{{pmid|23398157}}
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| style="text-align:center; background-color:hsla(180, 100%, 85%);" |'''Telomere attrition'''[[File:Telomeres transparent.png|frameless|88x88px]]
| style="text-align:center; background-color:hsla(180, 100%, 85%);" |'''[[Telomere Attrition|Telomere attrition]]'''[[File:Telomeres transparent.png|frameless|88x88px]]
| style="background-color:hsla(180, 100%, 85%);" |Telomere attrition refers to the progressive shortening of telomeres, which are protective sequences at the ends of chromosomes. This occurs due to the inability of DNA polymerases to completely replicate the ends of linear DNA, and the absence of telomerase in most somatic cells. Shortened telomeres lead to cellular aging and reduced regenerative capacity, manifesting as replicative senescence or Hayflick limit{{pmid|17024208}}. Shelterins protect telomeres but may mask damage leading to persistent DNA damage and cellular stress{{pmid|18680434}}. Dysfunctions in telomere maintenance are linked to various age-related diseases{{pmid|22965356}}.
| style="background-color:hsla(180, 100%, 85%);" |Telomere attrition refers to the progressive shortening of telomeres, which are protective sequences at the ends of chromosomes. This occurs due to the inability of DNA polymerases to completely replicate the ends of linear DNA, and the absence of telomerase in most somatic cells. Shortened telomeres lead to cellular aging and reduced regenerative capacity, manifesting as replicative senescence or Hayflick limit{{pmid|17024208}}. Shelterins protect telomeres but may mask damage leading to persistent DNA damage and cellular stress{{pmid|18680434}}. Dysfunctions in telomere maintenance are linked to various age-related diseases{{pmid|22965356}}.
|Telomere shortening is observed during normal aging in humans and mice{{pmid|17876321}}.
|Telomere shortening is observed during normal aging in humans and mice{{pmid|17876321}}.
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| style="text-align:center; background-color:hsla(210, 100%, 85%);" |'''Loss of proteostasis'''
| style="text-align:center; background-color:hsla(210, 100%, 85%);" |'''[[Loss of Proteostasis|Loss of proteostasis]]'''
'''[[File:Loss of Proteostasis.png|frameless|118x118px]]'''
'''[[File:Loss of Proteostasis.png|frameless|118x118px]]'''
| style="background-color:hsla(210, 100%, 85%);" |Loss of proteostasis refers to the disruption of the body's ability to regulate its proteins effectively, a process in which chaperones play a crucial role. This encompasses the processes of protein synthesis, folding, transport, and degradation. Chaperones, specialized proteins that assist in the proper folding and stabilization of other proteins, are essential in maintaining proteostasis. As we age, or in certain diseases, the balance of these processes can be disturbed, leading to the accumulation of misfolded or damaged proteins, and a decrease in the ability to produce and maintain healthy proteins. The decline in the efficiency or availability of chaperones contributes to this loss of proteostasis, exacerbating the accumulation of dysfunctional proteins and cellular stress.
| style="background-color:hsla(210, 100%, 85%);" |Loss of proteostasis refers to the disruption of the body's ability to regulate its proteins effectively, a process in which chaperones play a crucial role. This encompasses the processes of protein synthesis, folding, transport, and degradation. Chaperones, specialized proteins that assist in the proper folding and stabilization of other proteins, are essential in maintaining proteostasis. As we age, or in certain diseases, the balance of these processes can be disturbed, leading to the accumulation of misfolded or damaged proteins, and a decrease in the ability to produce and maintain healthy proteins. The decline in the efficiency or availability of chaperones contributes to this loss of proteostasis, exacerbating the accumulation of dysfunctional proteins and cellular stress.
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| style="text-align:center; background-color:hsla(0, 100%, 85%);" |'''Deregulated nutrient sensing'''[[File:Aiga restaurant knife-fork crossed.png|frameless|75x75px]]
| style="text-align:center; background-color:hsla(0, 100%, 85%);" |'''[[Deregulated Nutrient Sensing|Deregulated nutrient sensing]]'''[[File:Aiga restaurant knife-fork crossed.png|frameless|75x75px]]
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| style="text-align:center; background-color:hsla(0, 100%, 85%);" |'''Mitochondrial dysfunction'''[[File:Mitochondrion mini.svg|frameless|92x92px]]
| style="text-align:center; background-color:hsla(0, 100%, 85%);" |'''[[Mitochondrial Dysfunction|Mitochondrial dysfunction]]'''[[File:Mitochondrion mini.svg|frameless|92x92px]]
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| style="text-align:center; background-color:hsla(30, 100%, 85%);" |[[Senescent Cells|'''Cellular senescence''']][[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="text-align:center; background-color:hsla(30, 100%, 85%);" |[[Senescent Cells|'''Cellular senescence''']][[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]]
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| style="text-align:center; background-color:hsla(30, 100%, 85%);" |'''Stem cell exhaustion'''[[File:Stem cell differentiation.svg|frameless|106x106px]]
| style="text-align:center; background-color:hsla(30, 100%, 85%);" |'''[[Stem Cell Exhaustion|Stem cell exhaustion]]'''[[File:Stem cell differentiation.svg|frameless|106x106px]]
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| style="text-align:center; background-color:hsla(30, 100%, 85%);" |'''Dysbiosis'''
| style="text-align:center; background-color:hsla(30, 100%, 85%);" |'''[[Dysbiosis (Microbiome Disturbance)|Dysbiosis<br>(Microbiome disturbance)]]'''
'''(Microbiome disturbance)'''[[File:202004 Gut microbiota.svg|frameless|75x75px]]
[[File:202004 Gut microbiota.svg|frameless|75x75px]]
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| style="text-align:center; background-color:hsla(30, 100%, 85%);" |'''Chronic inflammation'''
| style="text-align:center; background-color:hsla(30, 100%, 85%);" |'''[[Chronic Inflammation (Inflammaging)|Chronic inflammation<br>(Inflammaging)]]'''
'''(Inflammaging)'''[[File:Histopathology of acute and chronic inflammation of the gastro-esophageal junction, annotated.jpg|frameless|75x75px]]
[[File:Histopathology of acute and chronic inflammation of the gastro-esophageal junction, annotated.jpg|frameless|75x75px]]
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| style="text-align:center; background-color:hsla(30, 100%, 85%);" |'''Altered intercellular communication'''[[File:Forms of Cell Signaling.png|frameless|75x75px]]
| style="text-align:center; background-color:hsla(30, 100%, 85%);" |'''[[Altered Intercellular Communication|Altered intercellular communication]]'''[[File:Forms of Cell Signaling.png|frameless|75x75px]]
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