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Functional Ageing > DNA Damaging and Senescence > Flashcards

DNA Damaging and Senescence Flashcards

1
Q

Give examples of species commonly used in a lab

A
  • C. elegans
  • rats
  • drosophila
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2
Q

What does stochastic mean?

A

the outcome is probable and can be influenced by genetics and environment

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3
Q

What does the wear and tear theory of ageing suggest?

A

ageing results from a gradual deterioration of the cells and tissues of the body via wear and tear, oxidative stress, exposure to radiation, toxins, or other deteriorative processes

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4
Q

Give examples of programmed theories of age

A
  • hormonal
  • programmed senescence
  • immunologic
  • telomere shortening
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5
Q

Give examples of stochastic theories of age

A
  • metabolic rate
  • glycation
  • somatic mutation
  • wear and tear
  • oxygen free radicals
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6
Q

What are ageotypes?

A

different types of ageing patterns in different individuals

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7
Q

What are the 9 hallmarks of ageing?

A
  • genomic instability
  • telomere attrition
  • epigenetic alterations
  • loss of proteostasis
  • dysregulated nutrient sensing
  • mitochondrial dysfunction
  • cellular senescence
  • stem cell exhaustion
  • altered intercellular communication
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8
Q

Give an example of functional connections between the hallmarks of ageing

A

telomere shortening leads to cellular senescence

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9
Q

What are the primary hallmarks of ageing?

A

causes of damage:
- loss of proteolysis
- epigenetic alterations
- telomere attrition
- genomic instability

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10
Q

What are the antagonistic hallmarks of ageing?

A

responses to damage:
- dysregulated nutrient sensing
- cellular senescence

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11
Q

What are the integrative hallmarks of ageing?

A

culprits of phenotypes:
- stem cell exhaustion
- altered intercellular communication

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12
Q

What is senescence?

A

a deteriorative process that follows development and maturation

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13
Q

What is replicative senescence?

A

when cells can no longer be replicated in culture

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14
Q

What is the primary role of senescence?

A

eliminating unwanted cells by inducing tissue remodelling

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15
Q

What are the 3 sequential processes involved in inducing tissue remodelling?

A
  1. stable proliferative arrest
  2. a secretory phenotype that recruits immune cells and modifies the ECM
  3. the mobilisation of nearby progenitors that populate the tissue
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16
Q

What are the 2 outcomes of cell cycle arrest?

A

stress relief or repair depending on the extent of damage or stress

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17
Q

What are the 2 types of senescence?

A

acute and chronic

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18
Q

What is acute senescence?

A

the scheduled clearance of unwanted cells e.g. wound healing, oncogene induced senescence (OIS), development (tissue patterning, cell plasticity)

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19
Q

What is chronic senescence?

A

when there is a gradual increase in stress over time and can happen in any cell that is dividing; it is unscheduled clearance of non-specific cells

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20
Q

What does early senescence involve?

A

lamin B1 downregulation, chromatin remodelling and SASP

21
Q

What does late (deep) senescence involve?

A

SASP moderation, retrotransposition, chromatin budding and histone proteolysis

22
Q

Give an example of when senescence can be beneficial

A

developmental processes e.g. neural tube closure

23
Q

What would happen if cells during brain development did not undergo senescence?

A

the brain would be enlarged and the embryos would die in utero

24
Q

Why do cataracts happen?

A

proteins within the lens begin to break down and vision becomes cloudy

25
Q

Give examples of senescence-related diseases

A
  • cancer
  • fibrosis
  • metabolic disorders
  • bone and cartilage disorders
26
Q

Where is disease-related senescence common?

A

in individuals who smoke since there is higher damage to the epithelial cells of the lungs

27
Q

Where is therapy-induced senescence common?

A
  • chemotherapy
  • kidney transplant
28
Q

What do commonly used markers of senescence derive from?

A

expansion and cell-cycle arrest stimuli

29
Q

Give examples of cell signals to arrest

A
  • epigenetic changes
  • DNA damage
  • cell-cycle inhibitors expression
  • HMGB1 nuclear exclusion
  • mitochondria
30
Q

Give examples of cell signals to expand

A
  • mitochondrial mass increase
  • karyomegaly
  • increase in cell soma size
31
Q

Give an example of pathways that regulate senescence-mediated arrest

A

DNA damage response from repair-resistant DNA segments with chromatin alterations reinforcing senesce (DNA-SCARS)

32
Q

What are the environmental factors that influence lifespan and ageing?

A
  • temperature
  • food availability
  • disposable soma theory
  • DNA repair capacity
33
Q

What is the disposable soma theory?

A

the correlation between longevity and the number of resources applied to somatic maintenance and repair

34
Q

What is Dauer?

A

an alternative stage of development whereby the larva goes into a type of stasis and can survive harsh conditions

35
Q

What is a consequence of DNA damage?

A

cell cycle arrest which can be temporary or permanent depending on the type and extent of damage

36
Q

What are the 3 tiers of defence against DNA damage?

A
  1. regulation of toxic molecules e.g. free radicals
  2. DNA repair
  3. pots-repair defence e.g. apoptosis or senescence
37
Q

What does BER deal with?

A

neurodegeneration

38
Q

What does mismatch repair deal with?

A

cancer

39
Q

Give examples of senescence signals

A
  • p53
  • p21
  • Rb
  • p16
40
Q

What are the 3 mechanisms by which DNA damage can drive ageing?

A
  • driving cells to senescence
  • exhausting regenerative capacity
  • impacting mitochondrial function
  • introducing protein aggregation
41
Q

How can cells be driven to senescence?

A

metabolism alterations, secretion of proinflammatory factors and local tissue environment alterations

42
Q

What does DNA damage drive?

A

ageing

43
Q

Give examples of molecular consequences of DNA damage

A
  • DNA/RNA polymerase stalling
  • dysfunctional telomeres
  • aneuploidy
44
Q

Give examples of cellular consequences of DNA damage

A
  • cellular senescence
  • stem cell exhaustion
45
Q

Give examples of systemic consequences of DNA damage

A
  • signalling mechanisms
  • inflammation
  • deregulated nutrient sensing
46
Q

What can DNA damage be?

A
  • exogenous (UV, chemicals, X-rays, chemotherapy)
  • endogenous (ROS, aldehydes, H2O)
47
Q

Give examples of how DNA repair defects accelerate human ageing

A
  • progeroid syndromes
  • osteoporosis in premature ageing systems
  • neurodegeneration
48
Q

Give examples of progeroid syndromes

A
  • Werner Syndrome
  • Bloom syndrome
  • Hutchison-Gilford progeria syndrome
49
Q

What happens once damage occurs/senescence kicks in?

A

there are very few functional cells; damaged/dysfunctional/senescent cells accumulate

Functional Ageing (4 decks)

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