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#049 - Clearing Zombie-Like Senescent Cells Reserves Signs of Aging - Professor Paul Robbins

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Content provided by humanOS Radio and Dan Pardi. All podcast content including episodes, graphics, and podcast descriptions are uploaded and provided directly by humanOS Radio and Dan Pardi or their podcast platform partner. If you believe someone is using your copyrighted work without your permission, you can follow the process outlined here https://ro.player.fm/legal.
Aging is arguably the leading risk factor for chronic diseases in the modern world. We have historically thought of aging as an inexorable decline of function, driven by the passage of time - something that we simply have to accept, and that cannot be changed. But what if aging were actually a modifiable risk factor? Your chronological age, meaning the length of time that you have been alive, obviously cannot be changed. But we know that biological aging can vary significantly, even among individuals who are of similar chronological age. If we can better understand the fundamental mechanisms that underlie biological aging, we might be able to devise interventions that could prevent or delay age-related diseases. One of the relevant processes is cellular senescence. Cellular senescence is a phenomenon through which normal cells irreversibly cease to divide in response to genomic damage. Senescent cells accumulate in the body as we get older, and they actually do a lot of bad stuff in the body. Senescent cells secrete pro-inflammatory factors, like cytokines, which induces a state of chronic low-grade inflammation. But it gets even worse. These senescent cells can also drive other healthy neighboring cells into senescence. So senescent cells are basically microscopic zombies! This has driven interest in identifying senolytics - compounds that can selectively kill senescent cells (while leaving normal cells alone). In this episode of humanOS Radio, Dan talks to Paul Robbins. Paul is the principal investigator at the Robbins Lab at Scripps Research Institute. Notably, his lab has been screening for drugs that can safely and effectively clear out senescent cells. This research has produced some remarkable results in animal models. For example, he and colleagues found that older mice that were given senolytics became faster and stronger, and experienced a 36% increased median post-treatment lifespan, compared to a control group. Wow! That’s just a tiny snapshot of this incredibly important work. To learn more, please check out the interview!
  continue reading

93 episoade

Artwork
iconDistribuie
 
Manage episode 219932478 series 1248550
Content provided by humanOS Radio and Dan Pardi. All podcast content including episodes, graphics, and podcast descriptions are uploaded and provided directly by humanOS Radio and Dan Pardi or their podcast platform partner. If you believe someone is using your copyrighted work without your permission, you can follow the process outlined here https://ro.player.fm/legal.
Aging is arguably the leading risk factor for chronic diseases in the modern world. We have historically thought of aging as an inexorable decline of function, driven by the passage of time - something that we simply have to accept, and that cannot be changed. But what if aging were actually a modifiable risk factor? Your chronological age, meaning the length of time that you have been alive, obviously cannot be changed. But we know that biological aging can vary significantly, even among individuals who are of similar chronological age. If we can better understand the fundamental mechanisms that underlie biological aging, we might be able to devise interventions that could prevent or delay age-related diseases. One of the relevant processes is cellular senescence. Cellular senescence is a phenomenon through which normal cells irreversibly cease to divide in response to genomic damage. Senescent cells accumulate in the body as we get older, and they actually do a lot of bad stuff in the body. Senescent cells secrete pro-inflammatory factors, like cytokines, which induces a state of chronic low-grade inflammation. But it gets even worse. These senescent cells can also drive other healthy neighboring cells into senescence. So senescent cells are basically microscopic zombies! This has driven interest in identifying senolytics - compounds that can selectively kill senescent cells (while leaving normal cells alone). In this episode of humanOS Radio, Dan talks to Paul Robbins. Paul is the principal investigator at the Robbins Lab at Scripps Research Institute. Notably, his lab has been screening for drugs that can safely and effectively clear out senescent cells. This research has produced some remarkable results in animal models. For example, he and colleagues found that older mice that were given senolytics became faster and stronger, and experienced a 36% increased median post-treatment lifespan, compared to a control group. Wow! That’s just a tiny snapshot of this incredibly important work. To learn more, please check out the interview!
  continue reading

93 episoade

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