Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiovascular System Module > Lecture 17 - Regulation Of Cardiac Senescence In Health And Disease > Flashcards

Lecture 17 - Regulation Of Cardiac Senescence In Health And Disease Flashcards

1
Q

How many people in the uk are living with heart and circulatory diseases?

A

7.4million

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the total annual health cost of heart and circulatory disease in the UK?

A

9 billion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What age is more likely to survive a heart attack - 50 or 85?

A

Someone who is 50

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is age related heart failure?

A

Decline in cardiac function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is at risk when a “healthy patient” has a heart attack?

A

Increased motility and increase in severity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are age-dependent changes that occur to cardiovascular tissues?

A

Diastolic dysfunction and systolic dysfunction and age remodelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is some examples of age remodelling?

A

Fibrosis, hypertrophy, decreased cardiomyocytes, inflammation, ischaemic areas and impaired regeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is accumulated cellular senescence associated with?

A

Age related tissue dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What happens when senescence cells are moved from a mouse?

A

They mouse is healthier and you get

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What type of expression is only seen in senescence cells?

A

P16

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is senescence cells driven by?

A

Cellular stress or replicated stress like telomeres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What can cause cellular stress?

A

DNA damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What do cytokindependent inhibitors do?

A

Make the cell exit the cell cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does SASP stand for?

A

Senescence associated secretory phenotype

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is antagonistic pleiotrophy?

A

A process that is beneficial earlier in life, it becomes detrimental in order life when there is no selective pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are examples of chronic senescence?

A

Replicative failure/stem cell dysfunction, tissue remodelling, inflammation and senescence propagation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What can senescence occur as a result as?

A

Persistent DDR - (DNA damage response)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are senescence cells casual to?

A

Age related pathophysiologies in multiple tissues and organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the pathophysiologies due to?

A

Cell cycle exit - effecting tissue homeostasis and regeneration and SASP - propagating the senescent phenotype and inducing tissue remodelling and inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What does cardiomyocyte senescence accumulate with?

A

Age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What happens when you induce senescence experimentally?

A

You get a young mouse with an old heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What happens if you over express genes in cardiomyocytes that delay senescence?

A

You delay the heart ageing process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Switch on senescence?

A

High heart ageing

24
Q

Switch off senescence?

A

Low heart ageing

25
Q

What do mouse models that demonstrate myocardial remodelling cause?

A

Myocardial remodelling characteristic of ageing

26
Q

What do the teleports protect during continuous cell proliferation?

A

Teleports protect the chromosome

27
Q

Where are telomeres found?

A

At the end of chromosomes

28
Q

What happens when a cell divides?

A

It replicates it DNA, every time you replicate the DNA you lose a bit from the end

29
Q

What happens to telomeres every time DNA is replicated?

A

Telomeres shorten

30
Q

What happens during stem cell dysfunction?

A

Exhaustion of the stem cell pool, reduced potential maintain tissue homeostasis

31
Q

What does both telomere shortening and stem cell dysfunction lead to?

A

Tissue degeneration

32
Q

What happens during a heart attack (as a post mitotic organ)?

A

Remodelling not regeneration, cardiomyocytes loss

33
Q

What is TAF?

A

Telomere associate DNA damage

34
Q

What are the stresses involved with TAF?

A

Oxidative stress

35
Q

What does TAF contribute to?

A

Senescent phenotype

36
Q

Does AF occur independently or dependently?

A

Independently of cell proliferation

37
Q

What is a persistent form of DNA damage?

A

TAF

38
Q

What are the favoured targets of persistent DNA damage?

A

Telomeres, if the damage occurs in the T region, the DNA damage response wont get in so wont be able to repair

39
Q

Does TAF accumulate during cardiomyocytes ageing?

A

There is an increase in TAFs in older individuals

40
Q

Could TAF contribute to senescence in a rarely cycling cardiomyocyte?

A

When you induce damage to the telomeres you get scenscence, TAF can occur independently of proliferation but itself can drive the senescence in the cardiomyocyte

41
Q

What effect does exit from the cell cycle have on the post mitotic heart?

A

It has little effect on the post mitotic heart

42
Q

What do senescent CMs produce?

A

A senescence associated secretory phenotype (SASP)

43
Q

What do aged cardiomyocyte express?

A

A non typical senescence associated secretory phenotype (SASP)

44
Q

What do secreted proteins up regulate in?

A

Aged cardiomyocytes

45
Q

What do secreted factors from cultured aged cardiomyocytes express?

A

They inhibit proliferation and promote expression of marks of myofibroblast differentiation/fibrosis

46
Q

What can senescence cardiac cells induce?

A

Senescence in other cells “bystander effect”

47
Q

What does TAFs lead to?

A

Expression of SASP which leads to fibrosis and inflammation

48
Q

What are senescent cells primed for?

A

Apoptosis

49
Q

What do inhibitors of senescence do?

A

Try to stop the apoptosis process

50
Q

What is hypertrophy reduced in?

A

Aged ink-ATTAC mice

51
Q

What is an example of a drug that clears senescence cells?

A

Navitoclax - reduces SASP and clears senescence cells

52
Q

What does navitoclax target?

A

Bcl2 to induce apoptosis

53
Q

What does navitoclax do?

A

It cleats senescent cells and attenuates myocardial remodelling in vivo.

54
Q

What are the benefits for navitoclax?

A

Fewer senescence cells, reduced fibrosis and hypertrophy

55
Q

What did pre-treatment with Navitoclax and then give subject a heart attack show?

A

Improved survival and recovery post heart attack

Cardiovascular System Module (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions