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In amputated limb samples kept alive outside the body, mouse tissue stalled in ordinary air while tadpole tissue kept rebuilding.<\/p>\n
Working at Ecole Polytechnique Federale de Lausanne (EPFL<\/a>), a team led by Can Aztekin linked that split to oxygen sensing rather than missing repair genes.<\/p>\n The researchers showed that mouse limbs could enter the same early program when oxygen dropped, which narrowed the gap sharply.<\/p>\n That did not produce a new leg, but it pushed the mystery back to the wound\u2019s opening decisions.<\/p>\n Oxygen sets the pace<\/p>\n After amputation, cells must seal exposed tissue quickly or scar-forming repair starts to crowd out rebuilding.<\/p>\n Low oxygen<\/a> stabilized HIF1A, a protein that helps cells sense oxygen, and that cue opened the door to regeneration.<\/p>\n Under higher oxygen, HIF1A broke down faster, so the mammalian program shut off before it could gather force.<\/p>\n That early fork helps explain how animals with many shared genes still end up healing in opposite ways.<\/p>\n Mouse cells wake up<\/p>\n Reduced oxygen made embryonic mouse limbs close faster and start forming the cell states linked to regrowth.<\/p>\n Skin cells became more mobile, which mattered because faster movement covered the wound before scar tissue could take over.<\/p>\n Metabolism also tilted toward glycolysis, a low-oxygen way to make energy, while gene-access patterns grew easier to open.<\/p>\n Those changes suggest mammals<\/a> fail early not because parts are missing, but because the starting conditions are wrong.<\/p>\n Frogs ignore the warning<\/p>\n Frog tadpole limbs kept regenerating even at 60 percent oxygen, a level that would stop mouse tissue cold.<\/p>\n Their cells held HIF1A steadier because they produced less of the machinery that normally shuts that pathway down.<\/p>\n Axolotl results fit the same pattern, which tied the finding to salamanders as well as frogs.<\/p>\n That consistency makes oxygen sensing look less like a quirk of one model and more like a common rule.<\/p>\n Mammals are not blank<\/p>\n Mammals do keep a narrow slice of regenerative ability, because injured digit tips<\/a> can sometimes grow back.<\/p>\n That exception matters because it shows the machinery is still there, even if most wounds never reach it.<\/p>\n Work on mouse digits found that softer tissue favors regrowth while stiffer tissue favors scarring.<\/p>\n Seen beside the oxygen work, that small success makes full limb loss look blocked rather than impossible.<\/p>\n Timing changes the answer<\/p>\n Age matters too, because frog tadpoles<\/a> lose much of this talent as they move toward adulthood.<\/p>\n Earlier work by Aztekin showed that older frog limbs fail when the wound cannot form the right surface tissue.<\/p>\n The study linked maturing limbs to signals that push repair away from regeneration and toward scarring.<\/p>\n The new oxygen result fits that timeline by showing one more way a promising wound can be derailed.<\/p>\n Humans fit the pattern<\/p>\n When the team compared frogs, axolotls, mice, and human data, the same divide kept showing up.<\/p>\n Human cells looked more like mouse<\/a> cells, with a stronger oxygen-sensing pattern likely to end regeneration early.<\/p>\n \u201cFor a long time, regeneration research focused on amphibians, while mammalian regeneration was rarely examined experimentally side by side in a comparable manner,\u201d said Aztekin.<\/p>\n That comparison matters because it treats human healing as part of the same biology, not a separate puzzle.<\/p>\n Promise with real limits<\/p>\n None of this amounts to a regrown mouse leg, and the researchers did not claim anything close.<\/p>\n What they triggered was the first stage, where wound closure, cell<\/a> behavior, and gene use all moved together.<\/p>\n \u201cBy directly comparing species that can and cannot regenerate, we bring a fresh perspective to a centuries-old question,\u201d Aztekin said.<\/p>\n The findings show that mammalian tissues can activate early regenerative processes, outlining a clear and testable path toward encouraging limb regrowth in adults.<\/p>\n What salamanders offer<\/p>\n Salamanders still stand apart among vertebrates<\/a> because they can replace tissues, organs, and whole limbs after injury.<\/p>\n A broad look at salamander limbs captured that record, which is why they remain the benchmark in regeneration biology.<\/p>\n The new work does not say mammals need salamander genes, only that one strong barrier may lie in oxygen sensing.<\/p>\n That reframes the problem from a vast evolutionary gulf to a cellular response that may be adjustable.<\/p>\n Across frogs, salamanders, mice, and human data, the message is that regeneration starts or stops in the wound\u2019s first oxygen reading.<\/p>\n Future work now has a sharper target: change oxygen sensing early enough, and mammalian healing may be nudged away from scarring.<\/p>\n The study is published in the journal Science<\/a>.<\/p>\n \u2014\u2013<\/p>\n Like what you read?\u00a0Subscribe to our newsletter<\/a>\u00a0for engaging articles, exclusive content, and the latest updates.<\/p>\n Check us out on\u00a0EarthSnap<\/a>, a free app brought to you by\u00a0Eric Ralls<\/a>\u00a0and Earth.com.<\/p>\n \u2014\u2013<\/p>\n","protected":false},"excerpt":{"rendered":"Scientists have found that a cell\u2019s response to oxygen helps decide why salamanders and tadpoles regrow limbs 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