A new study has suggested that “Zombie cells”, which are responsible for age-related illnesses, also heal damaged tissue. So, wiping them out might have major negative consequences.
Scientists call these “senescent cells” or zombies. They are cells that cease multiplying after stress or damage, but they don’t die. National Institute on Aging.
Instead, they release a host of molecules that stimulate immune cells and spark the development of immune cells. inflammation. The immune systemThese zombies are removed from the body by the immune system, but as we age it becomes less efficient. Cells accumulate, which causes inflammation, which contributes to the development of diseases like Cancer, Alzheimer’s disease, and osteoarthritis.
But zombie cells aren’t entirely bad.
New research, which was conducted in human cells and lab mice, shows that senescent cells can help with repair. lungTissue after injury by encouraging Stem cellsTo grow.
Killing these cells with dasatinib and quercetin (DQ) – a drug duo that’s been studied as a potential treatment to combat aging and age-related disease – disrupted this repair, the researchers reported 13 October in the journal Science.
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Senior author: “We aren’t the only lab to suggest senescence is a wound-healing process.” Tien PengAssociate professor of pulmonary and critical care allergy and sleep medicine at University of California, San Francisco.
A 2014 study in The Journal Developmental CellResearchers discovered that zombie cells can be used to heal skin wounds and that they can also be destroyed by “senolytics,” or zombie-slaying drugs.
Peng explained to Live Science that this suggests that senolytics may come with a price. The drugs must be able to block the bad effects of zombie cells without disrupting their good ones.
How “zombies” heal injured tissues
Researchers genetically modified mice to express a glowing protein that code for “p16,” which is often overactive in many senescent cell types, in order to find senescent lung cells.
A cell that switches on the gene would produce fluorescent proteins and begin to glow when it does.
Peng explained that the researchers used a technique to “really amplify this signal” and revealed cells with low levels of p16.
Soon after being born, glowing cells were found in the lungs of mice and their numbers increased throughout the rodent’s lives.
Fibroblasts are cells that make connective tissue as well as immune cell. The cells resided in a sheet-like structure called the “basement skin” which supports the lining of the air sacs and tubes. Blood vessels.
This sheet prevents harmful chemicals and pathogens entering the lungs, while allowing oxygen to enter the bloodstream.
This crucial interface is protected by the p16-carrying cells.
After injury, immune cells rush to repair the damage and release a series of signals that activate p16-carrying cell.
The number of immune cells increases and the fibroblasts release compounds that activate more immune cells. Stem cells growth.
The researchers discovered that DQ is able to stop the signaling cascade in mice and prevent stem cell growth.
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Moreover, p16-carrying cells extracted from donated human lungs can also promote stem cell growth – at least in lab dishes.
This suggests that DQ, as shown in mice, could also affect healing in humans.
“This combination treatment is currently available in multiple” Clinical trials“” and scientists have been looking for signs that senolytics interrupt healing, in general. Danny RohThe study was not conducted by a Boston University School of Medicine assistant professor of surgery who was not part of the research.
Roh shared this information with Live Science via email.
What does this mean for anti-aging drugs?
Although senolytics can slow down healing in the skin and lungs, some labs have discovered that they can speed up the healing of fractured bones. What’s the deal?
“Is bone any different to skin and lung? It could be, ” said Sundeep KhoslaMayo Clinic’s Osteoporosis, Bone Biology Laboratory leader, who was responsible for overseeing One of the earlier bone studies. Khosla prefers a different hypothesis.
Researchers gave the senolytics daily in the skin and lung studies. However, the breaks between doses were shorter in bone studies.
Khosla suggested that this strategy might hit the therapeutic sweet spot “where there’s enough inflammation to repair but not so much that you’re actually starting seeing negative effects.”
He said, “In terms clinical development of therapeutics the devil will be in the dosing.”
Khosla said that the study raises questions about which types of zombie cells senolytics are most effective at targeting.
Peng stated that senescence can be described as a dial rather than an on/off switch. Therefore, the spectrum of senescent cells is from least to most.
Peng and his collaborators are currently investigating the effects of zombies in old mice on healing.
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This article was first published by Live Science. Please read the Original article available here.
