7 ms·

New insights into transcription factors and chromatin remodeling

115 points by birriel 2y ago

tomrod 2y ago
... In mice.. And human! cells. From the paper: • Multi-omic analysis of maturation and aging across >45 mouse and human cell types • Common transcription factor pattern for chromatin remodeling in maturation and aging • Encoded via relative abundance of AP-1, CTCF, and cell identity factor binding sites • Remodeling mechanism activated by AP-1, stress, systemic factor, or PRC2 inhibition
jbandela1 2y ago
> “By pinpointing AP-1 as a master controller linked to aging across cell types, we can now study the effects of drugs that reduce its activity to extend quality of life,” he said [2]. Targeting AP-1 and its associated pathways could lead to interventions that slow down or even prevent the onset of these diseases, marking a significant advancement in geriatric medicine. Unfortunately, AP-1 is also involved in cancer. From https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10361657/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10361657/ > Activator protein-1 (AP-1) is a transcription factor that consists of a diverse group of members including Jun, Fos, Maf, and ATF. AP-1 involves a number of processes such as proliferation, migration, and invasion in cells. Dysfunctional AP-1 activity is associated with cancer initiation, development, invasion, migration and drug resistance. Mentioning AP-1 without mentioning its role in cancer is misleading. Many of the mechanisms that are involved with aging, likely have a role with controlling cancer by keeping cells, especially cells with damage, from proliferating or invading nearby or distant tissue.
- CuriouslyC 2y ago
  True, but we're getting a lot better at treating cancer, so I suspect that it is going to end up that we try to target it semi-selectively for life extension with the knowledge that it may cause cancer, then try to treat any cancers that emerge.
  - aflag 2y ago
    We're still terrible at treating cancer though. And the treatments very likely cause other health issues that can actually reduce life expectancy.
    - fzeroracer 2y ago
      We've massively improved in cancer treatment in just the past 20 years alone. Every year we get more and more precise with our ability to both map and target tumors, which in turn means less damage to the body as a whole during treatment and better odds of tumor elimination. This goes for both chemo and radiation.
  - Tade0 2y ago
    You'd need a particularly good (and cheap!) screening method to catch them before they become fatal. Digestive tract cancers in particular are often confused by patients with other, benign issues and are therefore diagnosed too late.
    - toomuchtodo 2y ago
      https://grail.com/ https://grail.com/ seems like the path we're on for that sort of screening (blood borne cancer biomarker surveillance)? AP-1 tweaks + mRNA and immunotherapy protocols for detected cancer + continued cancer screening developments might be a material longevity improvement. Typically, you're trying to die before any cancer gets you long term, so the need is to continually improve cancer detection and treatment. https://www.cancer.gov/about-cancer/treatment/types/biomarker-testing-cancer-treatment https://www.cancer.gov/about-cancer/treatment/types/biomarke... https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9074993/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9074993/
  - gumby 2y ago
    > we're getting a lot better at treating cancer, Is this really true? I know we are getting better in diagnosing cancers, so the time from initial diagnosis to death is longer, but it's not clear that overall lifespan of people with all cancers is any longer. If anything, because treatment starts sooner, quality of life may have diminshed. It is definitely true that treatments for some cancers have improved over the last couple of decades. I find the immunotherapies particularly exciting and seemingly promising. But in the broader cases I am not sure I could agree with your statement.
- futureshock 2y ago
  I have often heard it said that if we found a cure for cancer we would also get a cure for aging. The one immortal human I know is Henrietta Lacks (or her cancer rather).
  - jonathanlydall 2y ago
    Fascinating. https://en.wikipedia.org/wiki/Henrietta_Lacks https://en.wikipedia.org/wiki/Henrietta_Lacks
    - evanmoran 2y ago
      Amazingly, her immortal cell line was instrumental in polio eradication! https://en.wikipedia.org/wiki/HeLa#Polio_eradication https://en.wikipedia.org/wiki/HeLa#Polio_eradication
  - onlyrealcuzzo 2y ago
    I have heard that we age, primarily, to prevent ourselves from dying of cancer even faster than we already do. Animals that don't really age like the lobster, giant tortoise, bowhead whale, elephant, etc - also get cancer much less than we do.
    - jacobn 2y ago
      Is it known why/how those animals have reduced / negligible senescence? Like do they have some other variant of the AP-1 gene(s), or some such?
      - sterlind 2y ago
        one factor is how many copies of the p53 tumor suppressor gene they have. larger animals (with more cells) tend to have more copies of p53. p53 causes cells to self-destruct if they go off-script. many cancers have p53 mutations to thwart this. iirc senescence blocks damaged (potentially pre-cancerous) cells from reproducing, but unlike p53 doesn't kill them. replacing sensescent cells means more cell divisions, which also risks a cancerous mutation. so reducing senescence probably means making p53 more sensitive and redundant.
newzisforsukas 2y ago
https://www.sciencedirect.com/science/article/pii/S1550413124002316?via%3Dihub https://www.sciencedirect.com/science/article/pii/S155041312...
personalityson 2y ago
One step closer to longevity escape velocity
- ulf-77723 2y ago
  You mean a slower life is a longer life?
  - exe34 2y ago
    escape velocity in this context means that you stay at least one step ahead of dying, through medical advances, to the point that the first immortal human (at least one who will not die of old age) may have already been born.
    - throwaway290 2y ago
      [flagged]
      - kirubakaran 2y ago
        Pedantry is the cure for dying of old age
        throwaway290 2y ago
        believe it or not some would say accepting that people die of cancer or heart attacks rather than "old age" is actually key to tackling longevity :)
        exe34 2y ago
        it was a catch-all phrase, you muppet. we do know "old age" isn't a real disease, we do know about immortal jellyfish. we do know about strategies for engineered negligible senescence. it's not the gotcha you think you had.
gcp123 2y ago
The gist of it in plain english: 1. Our genes change as we age with some becoming more active, while others become less active. 2. The researchers found a special protein called AP-1 that acts like a master switch. As we get older, AP-1 becomes more active. 3. AP-1 turns on "adult" genes and turns down "young" genes. This happens in many different types of cells in our body. 4. These changes in gene activity are linked to the aging process and may explain why we experience age-related health issues. 5. Understanding this process could help scientists develop new ways to prevent or treat diseases that commonly affect older people, like Alzheimer's or diabetes.
- deleted 2y ago
  [deleted]
- spacephysics 2y ago
  Additionally there are cancer risks with modifying this process. Sounds similar to the telomere conundrum
  - throwaway743 2y ago
    What's the telomere conundrum?
- vikramkr 2y ago
  To clarify, they didn't "find a special protein called AP-1". AP-1 is a well known, well studied family of transcription factors. From snippet in background for https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6678392/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6678392/: "The Activator protein-1 (AP-1), is a group of transcription factors consisted of four sub-families: the Jun (c-Jun, JunB, JunD), Fos (c-Fos, FosB, Fra1, Fra2), Maf (musculoaponeurotic fibrosarcoma) (c-Maf, MafB, MafA. Mafg/f/k, Nrl), and the ATF-activating transcription factor (ATF2, LRF1/ATF3, BATF, JDP1, JDP2) protein families [21], characterized by pleiotropic effects and a central role in different aspects of the immune system such as T-cell activation, Th differentiation, T-cell anergy and exhaustion [22,23]. " They found a correlation between AP-1 binding sites/motifs and genes with age related changes in expression through their analysis (https://www.sciencedirect.com/science/article/pii/S1550413124002316?via%3Dihub https://www.sciencedirect.com/science/article/pii/S155041312...): "This revealed that age-opening DARs had the highest enrichment for a subset of bZIP motifs, including AP-1 subunits FRA2, FRA, JUN, JUNB, FOS, ATF3, and BATF, compared with the other peak categories (Figures 4C and S5B). Conversely, age-closing DARs had the lowest AP-1 enrichment (Figures 4C and S5B). As broadly expressed pioneer factors,39,40 AP-1 family members are responsive to a variety of stimuli41 and have been linked to potentiating age-related pathologies and phenotypes.12,13,42,43,44,45 This makes them strong candidates for driving age-related chromatin opening. Highly stable cCREs showed intermediate enrichment levels for these AP-1 motifs (Figures 4C and S5B). However, a distinct feature of highly stable cCREs was very high CTCF motif enrichment levels and binding relative to all other peak categories (Figures 4D, S5B, and S5C)."
hamandchris 2y ago
[flagged]
- Marcan 2y ago
  This comment doesn't belong on HN.
  - exe34 2y ago
    it'll be the end of history.
  - swayvil 2y ago
    I disagree. I think it totally belongs on HN. This method of censoring the unpopular. It can only lead to incest and mediocrity.
- ryandrake 2y ago
  Hilarious sarcasm, but a little scary to think about: The day someone actually invents medicine that reliably prevents death of old age, human culture will become permanently stuck, tied to that generation. Power, politics, science, wealth, art, and ideas in general, tend to change only when a generation dies and the next one gets a chance to flourish. "Science progresses one funeral at a time," and all that. People accumulate wealth and power, but only until they die. But if the dying part was solved, that final generation would simply accumulate unbounded, forever.
  - deleted 2y ago
    [deleted]
  - tstrimple 2y ago
    Lots of good sci-fi explore this topic. I'm a fan of the Altered Carbon novels. The super powerful are effectively immortal and are referred to as Meths for Methuselah.
  - chmod775 2y ago
    > People accumulate wealth and power, but only until they die. And their descendants continue right where they left off. It's not much of a difference to them simply not dying.
fifteen1506 2y ago
Oh great, everyone in positions of power will be Biden-like. That bodes well for society.
- jszymborski 2y ago
  W/o commenting on gerontocracies, this would mean that folks Biden's age wouldn't suffer as they do now from the deleterious effects of ageing. Put otherwise, Biden wouldn't be old at 81 if we completely understood the molecular biology of ageing. Unfortunately, we don't.
  - TaylorAlexander 2y ago
    Tho these people might not update their politics (I don’t have a sense that Biden ever did) and so while they may not suffer mental decline, we could find ourselves deprived of new thinking.
    - BriggyDwiggs42 2y ago
      We could always regulate that politically. An age limit for public service, though I guess that doesn’t cover most powerful people. Overall I hope that if we had figured out aging we’d be smart enough to deal with the consequences well but who knows.
      - TaylorAlexander 2y ago
        Hard to get the gerontocracy to vote against a gerontocracy. We can't even get proportional representation voting systems (at least not in the USA). Quite unfortunately, our system is built to protect the power of those who created it; it is not built to be smart.
1propionyl 2y ago
Unfortunately this site doesn't work properly with blockers enabled and redirect cycles. Unfortunately, won't be reading.
- qup 2y ago
  It works with curl
- Dudhbbh3343 2y ago
  Loads perfectly with Firefox for Android and uBlock.
boznz 2y ago
In my sixties and If longevity of life comes with full cognitive and physical health for the individual so they can continue contributing to society, then I'm all in. Otherwise what is the point, I will just be a burden on the world and reduced to a market for big pharma and big health care to get richer and the economy to get poorer as health care spending increases. I guess these are hard questions for everyone and I don't want individuals reduced to a number in a dataset but mankind has certainly gotten itself in a bit of a pickle.
swayvil 2y ago
It's like the world is some kind of clockwork. Or computer. Or a field of barley? What metaphor are we using these days?
begueradj 2y ago
It's strange that mitochondria is not mentioned in this article. For a long time, it was believed to play a paramount role in aging.
- vikramkr 2y ago
  It still is believed to play an important role in aging: https://www.nature.com/articles/s43587-022-00191-2 https://www.nature.com/articles/s43587-022-00191-2
grishka 2y ago
I wonder how this fits together with heterochronic parabiosis.
vikramkr 2y ago
Edit: Thanks to whoever changed the title for the post! jfc the media telephone chain here is absurd. "Revealing a master controller of development and ageing" becomes "AP-1: The Master Regulator." A -> the is a pretty big jump. (https://www.uq.edu.au/news/article/2024/06/revealing-master-controller-of-development-and-ageing https://www.uq.edu.au/news/article/2024/06/revealing-master-...) Also - ugh these content mills are so lame. The university PR departments aren't helping - why a university feels it needs to contribute to lowering public trust in science by claiming every paper is a generation defining breakthrough is beyond me. But maybe pause for a second before breathlessly passing along a headline like 'master controller of aging and development uncovered'? And the underlying research (https://www.sciencedirect.com/science/article/pii/S1550413124002316?via%3Dihub https://www.sciencedirect.com/science/article/pii/S155041312...) and techniques used etc is pretty interesting - please don't cut research funding to genetics a few years down the line when immortality fails to materialize like longevity.whatever promised.
Unbefleckt 2y ago
I'm sure I read about this in New Scientist maybe 12 years ago? They found this "switch" and turned it off in mice. We basically age and die so that we don't have denisovans running around mating with people who have hundreds of thousands of years of adaptations that have been tried and tested, but you can just turn that feature off. Right?
eointierney 2y ago
Having worked in cancer hospitals at the age of 16 (35 years ago) and having a father a doctor who coordinated long term cancer treatment in our country, I can say that cancer treatment has come on in leaps and bounds. What was once a death sentence is now likely treatable, and more treatments are coming online almost by the day. We will never beat cancer as we will never beat death, but we can prolong life, prevent pain, and always make sickness easier to bear both for those who suffer it and their loved ones. C'mon the Science!

115 points by birriel 2y ago

... In mice.. And human! cells. From the paper: • Multi-omic analysis of maturation and aging across >45 mouse and human cell types • Common transcription factor pattern for chromatin remodeling in maturation and aging • Encoded via relative abundance of AP-1, CTCF, and cell identity factor binding sites • Remodeling mechanism activated by AP-1, stress, systemic factor, or PRC2 inhibition

jbandela1 2y ago

> “By pinpointing AP-1 as a master controller linked to aging across cell types, we can now study the effects of drugs that reduce its activity to extend quality of life,” he said [2]. Targeting AP-1 and its associated pathways could lead to interventions that slow down or even prevent the onset of these diseases, marking a significant advancement in geriatric medicine. Unfortunately, AP-1 is also involved in cancer. From https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10361657/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10361657/ > Activator protein-1 (AP-1) is a transcription factor that consists of a diverse group of members including Jun, Fos, Maf, and ATF. AP-1 involves a number of processes such as proliferation, migration, and invasion in cells. Dysfunctional AP-1 activity is associated with cancer initiation, development, invasion, migration and drug resistance. Mentioning AP-1 without mentioning its role in cancer is misleading. Many of the mechanisms that are involved with aging, likely have a role with controlling cancer by keeping cells, especially cells with damage, from proliferating or invading nearby or distant tissue.

CuriouslyC 2y ago
True, but we're getting a lot better at treating cancer, so I suspect that it is going to end up that we try to target it semi-selectively for life extension with the knowledge that it may cause cancer, then try to treat any cancers that emerge.
- aflag 2y ago
  We're still terrible at treating cancer though. And the treatments very likely cause other health issues that can actually reduce life expectancy.
  - fzeroracer 2y ago
    We've massively improved in cancer treatment in just the past 20 years alone. Every year we get more and more precise with our ability to both map and target tumors, which in turn means less damage to the body as a whole during treatment and better odds of tumor elimination. This goes for both chemo and radiation.
- Tade0 2y ago
  You'd need a particularly good (and cheap!) screening method to catch them before they become fatal. Digestive tract cancers in particular are often confused by patients with other, benign issues and are therefore diagnosed too late.
  - toomuchtodo 2y ago
    https://grail.com/ https://grail.com/ seems like the path we're on for that sort of screening (blood borne cancer biomarker surveillance)? AP-1 tweaks + mRNA and immunotherapy protocols for detected cancer + continued cancer screening developments might be a material longevity improvement. Typically, you're trying to die before any cancer gets you long term, so the need is to continually improve cancer detection and treatment. https://www.cancer.gov/about-cancer/treatment/types/biomarker-testing-cancer-treatment https://www.cancer.gov/about-cancer/treatment/types/biomarke... https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9074993/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9074993/
- gumby 2y ago
  > we're getting a lot better at treating cancer, Is this really true? I know we are getting better in diagnosing cancers, so the time from initial diagnosis to death is longer, but it's not clear that overall lifespan of people with all cancers is any longer. If anything, because treatment starts sooner, quality of life may have diminshed. It is definitely true that treatments for some cancers have improved over the last couple of decades. I find the immunotherapies particularly exciting and seemingly promising. But in the broader cases I am not sure I could agree with your statement.
futureshock 2y ago
I have often heard it said that if we found a cure for cancer we would also get a cure for aging. The one immortal human I know is Henrietta Lacks (or her cancer rather).
- jonathanlydall 2y ago
  Fascinating. https://en.wikipedia.org/wiki/Henrietta_Lacks https://en.wikipedia.org/wiki/Henrietta_Lacks
  - evanmoran 2y ago
    Amazingly, her immortal cell line was instrumental in polio eradication! https://en.wikipedia.org/wiki/HeLa#Polio_eradication https://en.wikipedia.org/wiki/HeLa#Polio_eradication
- onlyrealcuzzo 2y ago
  I have heard that we age, primarily, to prevent ourselves from dying of cancer even faster than we already do. Animals that don't really age like the lobster, giant tortoise, bowhead whale, elephant, etc - also get cancer much less than we do.
  - jacobn 2y ago
    Is it known why/how those animals have reduced / negligible senescence? Like do they have some other variant of the AP-1 gene(s), or some such?
    - sterlind 2y ago
      one factor is how many copies of the p53 tumor suppressor gene they have. larger animals (with more cells) tend to have more copies of p53. p53 causes cells to self-destruct if they go off-script. many cancers have p53 mutations to thwart this. iirc senescence blocks damaged (potentially pre-cancerous) cells from reproducing, but unlike p53 doesn't kill them. replacing sensescent cells means more cell divisions, which also risks a cancerous mutation. so reducing senescence probably means making p53 more sensitive and redundant.

newzisforsukas 2y ago

https://www.sciencedirect.com/science/article/pii/S1550413124002316?via%3Dihub https://www.sciencedirect.com/science/article/pii/S155041312...

personalityson 2y ago

One step closer to longevity escape velocity

ulf-77723 2y ago
You mean a slower life is a longer life?
- exe34 2y ago
  escape velocity in this context means that you stay at least one step ahead of dying, through medical advances, to the point that the first immortal human (at least one who will not die of old age) may have already been born.
  - throwaway290 2y ago
    [flagged]
    - kirubakaran 2y ago
      Pedantry is the cure for dying of old age
      - throwaway290 2y ago
        believe it or not some would say accepting that people die of cancer or heart attacks rather than "old age" is actually key to tackling longevity :)
        exe34 2y ago
        it was a catch-all phrase, you muppet. we do know "old age" isn't a real disease, we do know about immortal jellyfish. we do know about strategies for engineered negligible senescence. it's not the gotcha you think you had.

gcp123 2y ago

The gist of it in plain english: 1. Our genes change as we age with some becoming more active, while others become less active. 2. The researchers found a special protein called AP-1 that acts like a master switch. As we get older, AP-1 becomes more active. 3. AP-1 turns on "adult" genes and turns down "young" genes. This happens in many different types of cells in our body. 4. These changes in gene activity are linked to the aging process and may explain why we experience age-related health issues. 5. Understanding this process could help scientists develop new ways to prevent or treat diseases that commonly affect older people, like Alzheimer's or diabetes.

deleted 2y ago
[deleted]
spacephysics 2y ago
Additionally there are cancer risks with modifying this process. Sounds similar to the telomere conundrum
- throwaway743 2y ago
  What's the telomere conundrum?
vikramkr 2y ago
To clarify, they didn't "find a special protein called AP-1". AP-1 is a well known, well studied family of transcription factors. From snippet in background for https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6678392/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6678392/: "The Activator protein-1 (AP-1), is a group of transcription factors consisted of four sub-families: the Jun (c-Jun, JunB, JunD), Fos (c-Fos, FosB, Fra1, Fra2), Maf (musculoaponeurotic fibrosarcoma) (c-Maf, MafB, MafA. Mafg/f/k, Nrl), and the ATF-activating transcription factor (ATF2, LRF1/ATF3, BATF, JDP1, JDP2) protein families [21], characterized by pleiotropic effects and a central role in different aspects of the immune system such as T-cell activation, Th differentiation, T-cell anergy and exhaustion [22,23]. " They found a correlation between AP-1 binding sites/motifs and genes with age related changes in expression through their analysis (https://www.sciencedirect.com/science/article/pii/S1550413124002316?via%3Dihub https://www.sciencedirect.com/science/article/pii/S155041312...): "This revealed that age-opening DARs had the highest enrichment for a subset of bZIP motifs, including AP-1 subunits FRA2, FRA, JUN, JUNB, FOS, ATF3, and BATF, compared with the other peak categories (Figures 4C and S5B). Conversely, age-closing DARs had the lowest AP-1 enrichment (Figures 4C and S5B). As broadly expressed pioneer factors,39,40 AP-1 family members are responsive to a variety of stimuli41 and have been linked to potentiating age-related pathologies and phenotypes.12,13,42,43,44,45 This makes them strong candidates for driving age-related chromatin opening. Highly stable cCREs showed intermediate enrichment levels for these AP-1 motifs (Figures 4C and S5B). However, a distinct feature of highly stable cCREs was very high CTCF motif enrichment levels and binding relative to all other peak categories (Figures 4D, S5B, and S5C)."

hamandchris 2y ago

[flagged]

Marcan 2y ago
This comment doesn't belong on HN.
- exe34 2y ago
  it'll be the end of history.
- swayvil 2y ago
  I disagree. I think it totally belongs on HN. This method of censoring the unpopular. It can only lead to incest and mediocrity.
ryandrake 2y ago
Hilarious sarcasm, but a little scary to think about: The day someone actually invents medicine that reliably prevents death of old age, human culture will become permanently stuck, tied to that generation. Power, politics, science, wealth, art, and ideas in general, tend to change only when a generation dies and the next one gets a chance to flourish. "Science progresses one funeral at a time," and all that. People accumulate wealth and power, but only until they die. But if the dying part was solved, that final generation would simply accumulate unbounded, forever.
- deleted 2y ago
  [deleted]
- tstrimple 2y ago
  Lots of good sci-fi explore this topic. I'm a fan of the Altered Carbon novels. The super powerful are effectively immortal and are referred to as Meths for Methuselah.
- chmod775 2y ago
  > People accumulate wealth and power, but only until they die. And their descendants continue right where they left off. It's not much of a difference to them simply not dying.

fifteen1506 2y ago

Oh great, everyone in positions of power will be Biden-like. That bodes well for society.

jszymborski 2y ago
W/o commenting on gerontocracies, this would mean that folks Biden's age wouldn't suffer as they do now from the deleterious effects of ageing. Put otherwise, Biden wouldn't be old at 81 if we completely understood the molecular biology of ageing. Unfortunately, we don't.
- TaylorAlexander 2y ago
  Tho these people might not update their politics (I don’t have a sense that Biden ever did) and so while they may not suffer mental decline, we could find ourselves deprived of new thinking.
  - BriggyDwiggs42 2y ago
    We could always regulate that politically. An age limit for public service, though I guess that doesn’t cover most powerful people. Overall I hope that if we had figured out aging we’d be smart enough to deal with the consequences well but who knows.
    - TaylorAlexander 2y ago
      Hard to get the gerontocracy to vote against a gerontocracy. We can't even get proportional representation voting systems (at least not in the USA). Quite unfortunately, our system is built to protect the power of those who created it; it is not built to be smart.

1propionyl 2y ago

Unfortunately this site doesn't work properly with blockers enabled and redirect cycles. Unfortunately, won't be reading.

qup 2y ago
It works with curl
Dudhbbh3343 2y ago
Loads perfectly with Firefox for Android and uBlock.

boznz 2y ago

In my sixties and If longevity of life comes with full cognitive and physical health for the individual so they can continue contributing to society, then I'm all in. Otherwise what is the point, I will just be a burden on the world and reduced to a market for big pharma and big health care to get richer and the economy to get poorer as health care spending increases. I guess these are hard questions for everyone and I don't want individuals reduced to a number in a dataset but mankind has certainly gotten itself in a bit of a pickle.

swayvil 2y ago

It's like the world is some kind of clockwork. Or computer. Or a field of barley? What metaphor are we using these days?

begueradj 2y ago

It's strange that mitochondria is not mentioned in this article. For a long time, it was believed to play a paramount role in aging.

vikramkr 2y ago
It still is believed to play an important role in aging: https://www.nature.com/articles/s43587-022-00191-2 https://www.nature.com/articles/s43587-022-00191-2

grishka 2y ago

I wonder how this fits together with heterochronic parabiosis.

vikramkr 2y ago

Edit: Thanks to whoever changed the title for the post! jfc the media telephone chain here is absurd. "Revealing a master controller of development and ageing" becomes "AP-1: The Master Regulator." A -> the is a pretty big jump. (https://www.uq.edu.au/news/article/2024/06/revealing-master-controller-of-development-and-ageing https://www.uq.edu.au/news/article/2024/06/revealing-master-...) Also - ugh these content mills are so lame. The university PR departments aren't helping - why a university feels it needs to contribute to lowering public trust in science by claiming every paper is a generation defining breakthrough is beyond me. But maybe pause for a second before breathlessly passing along a headline like 'master controller of aging and development uncovered'? And the underlying research (https://www.sciencedirect.com/science/article/pii/S1550413124002316?via%3Dihub https://www.sciencedirect.com/science/article/pii/S155041312...) and techniques used etc is pretty interesting - please don't cut research funding to genetics a few years down the line when immortality fails to materialize like longevity.whatever promised.

Unbefleckt 2y ago

I'm sure I read about this in New Scientist maybe 12 years ago? They found this "switch" and turned it off in mice. We basically age and die so that we don't have denisovans running around mating with people who have hundreds of thousands of years of adaptations that have been tried and tested, but you can just turn that feature off. Right?

eointierney 2y ago

Having worked in cancer hospitals at the age of 16 (35 years ago) and having a father a doctor who coordinated long term cancer treatment in our country, I can say that cancer treatment has come on in leaps and bounds. What was once a death sentence is now likely treatable, and more treatments are coming online almost by the day. We will never beat cancer as we will never beat death, but we can prolong life, prevent pain, and always make sickness easier to bear both for those who suffer it and their loved ones. C'mon the Science!