logo
Dying Cells Play a Vital, Unexpected Role in Healing, Study Shows

Dying Cells Play a Vital, Unexpected Role in Healing, Study Shows

Yahoo05-04-2025
A new study reveals some surprising discoveries about healing processes that are potentially triggered by the process of necrosis, or premature cell death.
Necrosis can be triggered by illness or injury – causing significant damage after heart attacks and strokes, for example. It's a messy death for cells and tissue, unlike the planned cell death called apoptosis that's a healthy part of the biological cycle.
When studying necrosis in fruit flies (Drosophila melanogaster, well known for their regenerative capabilities), a team of researchers at Arizona State University (ASU) noticed something unexpected: in their dying moments, cells surrounding those hit by necrosis send out signals encouraging cell growth in healthier parts of the tissue.
This is done by triggering the production of enzymes known as caspases. In apoptosis, caspases act as executioners, but when summoned by necrosis across relatively long distances, another type of caspase appears to promote healing in certain cells instead.
"This finding is significant because it not only adds to the body of evidence that caspases are involved in signaling events that promote repair, but also shows for the first time that this phenomenon occurs following necrosis," says geneticist and developmental biologist Rob Harris of ASU.
The new research builds on a 2021 study in which some of the same researchers noticed necrosis-affected cells sending out signals – not just to the cells surrounding the tissue damage, but to other unaffected cells farther away. These latest findings help to add more clarity about what exactly is happening.
And while we haven't seen this happen in humans yet, and our bodies are much more complex than those of fruit flies, if we can gain a better understanding of this process, then we may be able to investigate harnessing it to facilitate our own healing.
The researchers are hopeful that the newly discovered Necrosis-induced Caspase Positive (NiCP) cells can teach us more about tissue regeneration and wound repair. Only some of the caspase-enabled cells reacting to necrosis survived though. Knowing the reasons for this will be an important next step.
"Altogether, our latest findings suggest a model in which necrotic injuries induce caspase activity in cells at a distance from an injury," says research technician Chloe Van Hazel of ASU.
It's still early days for this research, but it's an intriguing discovery in the field of tissue repair and regeneration, and the molecular processes behind it, and how those processes (like caspase function) can adapt based on context.
As a species, we're pretty good at fixing ourselves up, but we could do better, especially as we get older. It's possible that this is something our bodies have become worse at as we have evolved over time, but relearning these skills could have profound health impacts.
"Our findings reinforce the idea that there is much more to be understood about the role of caspases in tissue repair," says Harris.
"For now, they reveal an important genetic response to cell death that could potentially be leveraged to augment the regeneration of necrotic wounds."
The research has been published in eLIfe.
Does Added Protein Really Enhance The Nutrition of Your Food?
A Week of Swimming in Cold Water Can Change You on a Cellular Level
How You Hear May Have More to Do With Your Sex Than Your Age
Orange background

Try Our AI Features

Explore what Daily8 AI can do for you:

Comments

No comments yet...

Related Articles

Surprise Discovery About Sugar in The Brain Could Help Fight Alzheimer's
Surprise Discovery About Sugar in The Brain Could Help Fight Alzheimer's

Yahoo

time08-07-2025

  • Yahoo

Surprise Discovery About Sugar in The Brain Could Help Fight Alzheimer's

Stores of glucose in the brain could play a much more significant role in the pathological degeneration of neurons than scientists realized, opening the way to new treatments for conditions like Alzheimer's disease. Alzheimer's is a tauopathy; a condition characterized by harmful build-ups of tau proteins inside neurons. It's not clear, however, if these build-ups are a cause or a consequence of the disease. A new study now adds important detail by revealing significant interactions between tau and glucose in its stored form of glycogen. Led by a team from the Buck Institute for Research on Aging in the US, the research sheds new light on the functions of glycogen in the brain. Before now, it's only been regarded as an energy backup for the liver and the muscles. "This new study challenges that view, and it does so with striking implications," says molecular biologist Pankaj Kapahi, from the Buck Institute. "Stored glycogen doesn't just sit there in the brain, it is involved in pathology." Related: Building on links previously found between glycogen and neurodegeneration, the researchers spotted evidence of excessive glycogen levels both in tauopathy models created in fruit flies (Drosophila melanogaster) and in the brain cells of people with Alzheimer's. Further analysis revealed a key mechanism at play: tau proteins interrupt the normal breakdown and use of glycogen in the brain, adding to the dangerous build-up of both tau and glycogen, as well as lowering protective neuron defense barriers. Crucial to this interaction is the activity of glycogen phosphorylase or GlyP, the main enzyme tasked with turning glycogen into a fuel the body can use. When the researchers boosted GlyP production in fruit flies, glycogen stores were utilized once more, helping to fight back against cell damage. "By increasing GlyP activity, the brain cells could better detoxify harmful reactive oxygen species, thereby reducing damage and even extending the lifespan of tauopathy model flies," says Buck Institute biologist Sudipta Bar. The team wondered if a restricted diet – already associated with better brain health – would help. When fruit flies affected by tauopathy were put on a low-protein diet, they lived longer and showed reduced brain damage, suggesting that the metabolic shift prompted by dieting can help boost GlyP. It's a notable set of findings, not least because it suggests a way that glycogen and tau aggregation could be tackled in the brain. The researchers also developed a drug based around the 8-Br-cAMP molecule to mimic the effects of dietary restriction, which had similar effects on flies in experiments. The work might even tie into research involving GLP-1 receptor agonists such as Ozempic, designed to manage diabetes and reduce weight, but also now showing promise for protecting against dementia. That might be because these drugs interact with one of glycogen's pathways, the researchers suggest. "By discovering how neurons manage sugar, we may have unearthed a novel therapeutic strategy: one that targets the cell's inner chemistry to fight age-related decline," says Kapahi. "As we continue to age as a society, findings like these offer hope that better understanding – and perhaps rebalancing – our brain's hidden sugar code could unlock powerful tools for combating dementia." The research has been published in Nature Metabolism. Air Pollution 'Strongly Associated' With DNA Mutations Tied to Lung Cancer FDA Issues Warning Over Dangerous 'Gas Station Heroin' Substance Mysterious Leprosy Pathogen Has Lurked in The Americas For 4,000 Years

Surprise Discovery About Sugar in The Brain Could Help Fight Alzheimer's
Surprise Discovery About Sugar in The Brain Could Help Fight Alzheimer's

Yahoo

time08-07-2025

  • Yahoo

Surprise Discovery About Sugar in The Brain Could Help Fight Alzheimer's

Stores of glucose in the brain could play a much more significant role in the pathological degeneration of neurons than scientists realized, opening the way to new treatments for conditions like Alzheimer's disease. Alzheimer's is a tauopathy; a condition characterized by harmful build-ups of tau proteins inside neurons. It's not clear, however, if these build-ups are a cause or a consequence of the disease. A new study now adds important detail by revealing significant interactions between tau and glucose in its stored form of glycogen. Led by a team from the Buck Institute for Research on Aging in the US, the research sheds new light on the functions of glycogen in the brain. Before now, it's only been regarded as an energy backup for the liver and the muscles. "This new study challenges that view, and it does so with striking implications," says molecular biologist Pankaj Kapahi, from the Buck Institute. "Stored glycogen doesn't just sit there in the brain, it is involved in pathology." Related: Building on links previously found between glycogen and neurodegeneration, the researchers spotted evidence of excessive glycogen levels both in tauopathy models created in fruit flies (Drosophila melanogaster) and in the brain cells of people with Alzheimer's. Further analysis revealed a key mechanism at play: tau proteins interrupt the normal breakdown and use of glycogen in the brain, adding to the dangerous build-up of both tau and glycogen, as well as lowering protective neuron defense barriers. Crucial to this interaction is the activity of glycogen phosphorylase or GlyP, the main enzyme tasked with turning glycogen into a fuel the body can use. When the researchers boosted GlyP production in fruit flies, glycogen stores were utilized once more, helping to fight back against cell damage. "By increasing GlyP activity, the brain cells could better detoxify harmful reactive oxygen species, thereby reducing damage and even extending the lifespan of tauopathy model flies," says Buck Institute biologist Sudipta Bar. The team wondered if a restricted diet – already associated with better brain health – would help. When fruit flies affected by tauopathy were put on a low-protein diet, they lived longer and showed reduced brain damage, suggesting that the metabolic shift prompted by dieting can help boost GlyP. It's a notable set of findings, not least because it suggests a way that glycogen and tau aggregation could be tackled in the brain. The researchers also developed a drug based around the 8-Br-cAMP molecule to mimic the effects of dietary restriction, which had similar effects on flies in experiments. The work might even tie into research involving GLP-1 receptor agonists such as Ozempic, designed to manage diabetes and reduce weight, but also now showing promise for protecting against dementia. That might be because these drugs interact with one of glycogen's pathways, the researchers suggest. "By discovering how neurons manage sugar, we may have unearthed a novel therapeutic strategy: one that targets the cell's inner chemistry to fight age-related decline," says Kapahi. "As we continue to age as a society, findings like these offer hope that better understanding – and perhaps rebalancing – our brain's hidden sugar code could unlock powerful tools for combating dementia." The research has been published in Nature Metabolism. Air Pollution 'Strongly Associated' With DNA Mutations Tied to Lung Cancer FDA Issues Warning Over Dangerous 'Gas Station Heroin' Substance Mysterious Leprosy Pathogen Has Lurked in The Americas For 4,000 Years

DOWNLOAD THE APP

Get Started Now: Download the App

Ready to dive into a world of global content with local flavor? Download Daily8 app today from your preferred app store and start exploring.
app-storeplay-store