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Hallmarks of Aging: Difference between revisions
→The Hallmarks in Detail
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== The Hallmarks in Detail == | == The Hallmarks in Detail == | ||
{| class="wikitable" | {| class="wikitable" | ||
! | !Hallmark | ||
! Background | ! Background | ||
!Manifests during normal aging | !Manifests during normal aging | ||
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!Associated human diseases | !Associated human diseases | ||
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| style="text-align:center; background-color:hsla(180, 100%, 85%);" |[[File:DNA Structure+Key+Labelled.pn NoBB.png|frameless|76x76px]] | | style="text-align:center; background-color:hsla(180, 100%, 85%);" |'''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%);" |[[File:Telomeres transparent.png|frameless|88x88px]] | | style="text-align:center; background-color:hsla(180, 100%, 85%);" |'''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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|Telomere shortening is associated with a variety of human diseases, including pulmonary fibrosis, dyskeratosis congenita, and aplastic anemia, often linked to deficiencies in telomerase or shelterin components{{pmid|22965356}}. | |Telomere shortening is associated with a variety of human diseases, including pulmonary fibrosis, dyskeratosis congenita, and aplastic anemia, often linked to deficiencies in telomerase or shelterin components{{pmid|22965356}}. | ||
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| rowspan="4" style="text-align:center; background-color:hsla(180, 100%, 85%);" |[[File:Epigenome-transparent-upscale.png|frameless|85x85px]] | | rowspan="4" style="text-align:center; background-color:hsla(180, 100%, 85%);" |'''[[Epigenetic Alterations|Epigenetic alterations]]'''[[File:Epigenome-transparent-upscale.png|frameless|85x85px]] | ||
| style="background-color:hsla(180, 100%, 85%);" |'''Histone modifications''' are a type of epigenetic alteration that play a crucial role in regulating gene expression. Histones are proteins around which DNA is wrapped in eukaryotic cells, forming a structure known as a nucleosome. These modifications occur primarily at the tails of histone proteins and influence how tightly or loosely DNA is wound around the histones, affecting the accessibility of the DNA to various cellular machinery for processes like transcription, replication, and repair. | | style="background-color:hsla(180, 100%, 85%);" |'''Histone modifications''' are a type of epigenetic alteration that play a crucial role in regulating gene expression. Histones are proteins around which DNA is wrapped in eukaryotic cells, forming a structure known as a nucleosome. These modifications occur primarily at the tails of histone proteins and influence how tightly or loosely DNA is wound around the histones, affecting the accessibility of the DNA to various cellular machinery for processes like transcription, replication, and repair. | ||
|Chemical changes to histone proteins after they are formed can activate or silence gene expression and regulate the aging process.{{pmid|17320507}} | |Chemical changes to histone proteins after they are formed can activate or silence gene expression and regulate the aging process.{{pmid|17320507}} | ||
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| style="text-align:center; background-color:hsla(210, 100%, 85%);" |[[File:Stress signaling.png|frameless|95x95px]] | | style="text-align:center; background-color:hsla(210, 100%, 85%);" |'''Loss of proteostasis'''[[File:Stress signaling.png|frameless|95x95px]] | ||
| style="background-color:hsla(210, 100%, 85%);" | | | 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="text-align:center; background-color:hsla(210, 100%, 85%);" |'''Disabled autophagy'''[[File:Macro-micro-autophagy.gif|frameless|101x101px]] | ||
| style="background-color:hsla(210, 100%, 85%);" | | | 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="text-align:center; background-color:hsla(0, 100%, 85%);" |'''Deregulated nutrient sensing'''[[File:Aiga restaurant knife-fork crossed.png|frameless|75x75px]] | ||
| style="background-color:hsla(0, 100%, 85%);" | | | style="background-color:hsla(0, 100%, 85%);" | | ||
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| style="text-align:center; background-color:hsla(0, 100%, 85%);" |[[File:Mitochondrion mini.svg|frameless|92x92px]] | | style="text-align:center; background-color:hsla(0, 100%, 85%);" |'''Mitochondrial dysfunction'''[[File:Mitochondrion mini.svg|frameless|92x92px]] | ||
| style="background-color:hsla(0, 100%, 85%);" | | | style="background-color:hsla(0, 100%, 85%);" | | ||
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| style="text-align:center; background-color:hsla(30, 100%, 85%);" |[[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]] | ||
| style="background-color:hsla(30, 100%, 85%);" | | | style="background-color:hsla(30, 100%, 85%);" | | ||
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| style="text-align:center; background-color:hsla(30, 100%, 85%);" |[[File:Stem cell differentiation.svg|frameless|106x106px]] | | style="text-align:center; background-color:hsla(30, 100%, 85%);" |'''Stem cell exhaustion'''[[File:Stem cell differentiation.svg|frameless|106x106px]] | ||
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| style="text-align:center; | | style="text-align:center; background-color:hsla(30, 100%, 85%);" |'''Dysbiosis''' | ||
'''(Microbiome disturbance)'''[[File:202004 Gut microbiota.svg|frameless|75x75px]] | |||
'''(Microbiome disturbance)''' | |||
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| style="text-align:center; background-color:hsla(30, 100%, 85%);" |[[File:Histopathology of acute and chronic inflammation of the gastro-esophageal junction, annotated.jpg|frameless|75x75px]] | | style="text-align:center; background-color:hsla(30, 100%, 85%);" |'''Chronic inflammation''' | ||
'''(Inflammaging)'''[[File:Histopathology of acute and chronic inflammation of the gastro-esophageal junction, annotated.jpg|frameless|75x75px]] | |||
| style="background-color:hsla(30, 100%, 85%);" | | | style="background-color:hsla(30, 100%, 85%);" | | ||
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| style="text-align:center; background-color:hsla(30, 100%, 85%);" |[[File:Forms of Cell Signaling.png|frameless|75x75px]] | | style="text-align:center; background-color:hsla(30, 100%, 85%);" |'''Altered intercellular communication'''[[File:Forms of Cell Signaling.png|frameless|75x75px]] | ||
| style="background-color:hsla(30, 100%, 85%);" | | | style="background-color:hsla(30, 100%, 85%);" | | ||
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