Scientists uncover a cellular survival mechanism that helps severely damaged tissue regenerate and may also reveal why some cancers return after treatment. Tissues such as skin, along with the epithelial layers that cover and line many organs, have a remarkable ability to rebuild themselves after extensive damage. Scientists have known about this response, called compensatory proliferation, for roughly half a century.
Yet exactly how cells manage to trigger such dramatic regrowth has remained a mystery. The phenomenon was first documented in the 1970s, when researchers exposed fly larvae to high doses of radiation. Despite major damage to epithelial tissue, the larvae were able to regenerate fully functional wings.
Similar regenerative responses have since been observed across many species, including humans. Now, researchers at the Weizmann Institute of Science say they have identified a molecular mechanism that helps explain how this process works. Their study, published in Nature Communications, points to a surprising role for caspases, enzymes best known for helping destroy cells.
Instead of simply promoting cell death, caspases can apparently help certain cells become resistant to death. Those survivors can then participate in rebuilding damaged tissue and may even become better equipped to withstand future injury. The same ability, however, could have a dangerous downside.
Cancer cells may exploit this survival mechanism, potentially contributing to tumors that return in a more aggressive and treatment-resistant form. The discovery could eventually help researchers develop approaches that encourage healthy tissue repair while also reducing the risk of cancer recurrence. When Cell Death Machinery Promotes Survival One of the main ways the body eliminates unwanted cells is through apoptosis, a carefully controlled form of cellular "suicide." Cells can enter apoptosis when they become old, damaged, or receive molecular signals telling them that their time is up.
The process involves several caspase enzymes. An initiator caspase first activates the pathway, followed by effector caspases that break apart proteins inside the doomed cell. During the past two decades, however, researchers have discovered that apoptotic caspases are not limited to killing cells.
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