Texas A&M University-ийн судлаачид хөхтөн амьтдын эд эрхтнийг гаднын үүдэл эс ашиглалгүйгээр, химийн аргаар нөхөн сэргээх шинэ аргыг туршилтаар баталлаа.
Nature Communications сэтгүүлд нийтлэгдсэн судалгаагаар, эдгээр амьтны биед гэмтлийн дараа үүсдэг сорвижилтыг өөрчилж, яс, үе мөч, шөрмөс үүсгэх чадвартай “бластема” (blastema) эсийг идэвхжүүлэх боломжтойг тогтоожээ. Уг процесс нь хөхтөн амьтдад нөхөн төлжих чадвар байхгүй биш, харин унтаа байдалд байдаг гэсэн дүгнэлтэд хүргэв.
Судлаачид шархны эдгэрэлтийн дараа фибробласт эсүүдийг чиглүүлэх замаар энэхүү үйл явцыг удирдсан байна. Эхлээд “fibroblast growth factor 2” (FGF2) уургийг ашиглан эсийн бөөгнөрлийг үүсгэж, дараа нь “bone morphogenetic protein 2” (BMP2) уураг нэмснээр шинэ яс, үе мөч, холбоос эдүүд бүрэлджээ. Энэхүү үр дүн нь өмнө нь зөвхөн гүрвэл зэрэг нөхөн төлжих чадвар өндөртэй амьтдад ажиглагддаг байсан үзэгдэл юм.
Судалгааны багийн ахлагч, доктор Кен Мунеока болон түүний хамтрагч доктор Ларри Сува нарын тайлбарласнаар, шархны эдгэрэлтийн үед сорви үүсгэдэг эсүүдийг зөв молекул дохиогоор өдөөхөд нөхөн төлжилтийн үйл явцад шилжүүлэх боломжтой аж. Энэхүү арга нь хөхтөн амьтны эд эрхтнийг нөхөн сэргээх эмчилгээний салбарт цоо шинэ боломжийг нээж байгаа бөгөөд одоогоор хэрэглэгдэж буй зарим эм бэлдмэлүүдтэй ижил төстэй уургуудыг ашигласан нь эмнэлзүйн туршилтад орох гарцыг хялбарчилж магадгүй юм.
Дэлгэрэнгүйг эх сурвалжаас харах
↓Эх сурвалжийг нээх ↓
For the first time in a mammal, researchers have chemically coaxed wound cells into forming new bone, joints, tendons, and ligaments after amputation, without adding any external stem cells. The work, published in Nature Communications by a team at Texas A&M University, demonstrates that the regenerative capacity long considered absent in mammals may simply be dormant, and that two growth factor proteins applied in sequence are enough to activate it.
The study focused on a structure called a blastema: a mass of proliferating, undifferentiated cells that forms at an amputation site in highly regenerative animals like salamanders, and serves as the raw material for rebuilding lost structures. Mammals do not normally produce a blastema after injury. Instead, the body seals the wound through fibrosis, a process in which fibroblast cells lay down collagen and fibronectin to close the site quickly. The Texas A&M team found a way to push those same cells in a different direction.
Two Proteins Applied in Sequence Produced a Structure Mammals Shouldn’t Be Able to Form
The protocol begins after the wound has already closed. Researchers applied fibroblast growth factor 2 (FGF2) first, which stimulated the formation of a blastema-like cell mass at the site, something that does not occur in mammals under normal healing conditions.
Several days later, they applied bone morphogenetic protein 2 (BMP2), which signaled those cells to begin constructing new tissue. The result was a regenerated digit that included two new bone elements, a synovial joint, tendon, and ligament tissue from the stump, and a newly formed ligament connecting the two ectopic bones.
“We regenerated what you would expect to see at that level of injury,” said Dr. Ken Muneoka, the study’s lead researcher. “The structures are there, just not in a perfect form.” The regenerated elements were incomplete compared to the original anatomy, but their presence represents a category of outcome that mammalian biology was not thought capable of producing.
The Cells That Close Wounds Are the Same Ones That Could Rebuild Tissue
A central finding of the study is that regeneration does not require importing external stem cells, which is the basis of many current regenerative medicine approaches. The fibroblasts already present at a mammalian wound site appear to retain the potential to form a blastema, if given the right molecular signal at the right time.
“It’s as if these cells can move in two different directions,” Muneoka said. “They could either make a scar or make a blastema. Our research focused on redirecting the behavior of fibroblasts already present at the injury site.” Dr. Larry Suva, a co-investigator on the study, framed it similarly: “The cells that we thought to be unprogrammable, in fact are. The capacity is not absent, it’s just obscured.”
The study also demonstrated what researchers call positional re-specification: cells were redirected to form structures in locations beyond where those structures originally existed. This kind of spatial reprogramming is well documented in developmental biology but had not previously been observed as a response to injury in a mammalian model.
Blastema Genetics May Point Toward Shared Mechanisms Across Species
The blastema concept has been studied most closely in animals with strong whole-body regenerative capacity. A 2024 Nature Communications study on fragmenting potworms (Enchytraeus japonensis) identified two genes, soxC and mmpReg, as key drivers of blastema formation in that species.
The researchers also found similar expression dynamics of SoxC orthologues during frog tadpole tail regeneration, raising the possibility that the molecular machinery underlying blastema formation has been conserved across a broader range of animals than previously understood, including, potentially, mammals that simply no longer activate it.
In mammals, the normal wound response works against this. When tissue is damaged, platelets form clots, immune cells clear debris, and fibroblasts proliferate to deposit scar material. The American Liver Foundation describes the same fibrotic mechanism in the context of liver disease, where repeated scarring in place of regeneration progressively impairs organ function. The parallel illustrates a broader principle: fibrosis is fast and reliable, but it forecloses the more structurally complex outcome that blastema formation makes possible.
The regulatory path for clinical testing may already be shorter than expected
Full limb regrowth in humans is not what this research is targeting, at least not yet. Muneoka has pointed to more immediate clinical possibilities, particularly for conditions where the balance between scarring and regeneration has direct consequences, such as amputation recovery and musculoskeletal repair. “People should start thinking about using these signals during the healing process,” he said. “Even shifting the response slightly away from scarring could have real benefits.”
The two proteins used in the study are not experimental compounds. BMP2 already holds FDA approval for certain orthopedic applications, and FGF2 is currently in multiple clinical trials. That existing regulatory history may reduce the barrier to testing this sequential approach in human contexts, though the jump from a mouse digit model to clinical use involves substantial additional work. “This changes the way we think about what’s possible,” Suva said. “Once you show that regeneration can be activated, it opens the door to asking entirely new questions.”
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