Dead-cell DNA slows skin recovery

This hypothesis asks why equal stress, timed differently, might slow recovery in middle-aged skin. It proposes two carriers. Nuclear DNA from dead cells could join chromosomes in surviving fibroblasts, skin support cells. Or mineral particles could persist in the extracellular matrix, material between cells. The test reorders equal stress across biological phases, then gives reconstructed skin a final challenge. Slower recovery retained by purified fibroblasts on fresh nonmineralized matrix, with confirmed DNA/chromosome junctions and cell fusion excluded as the cause, would support the DNA mechanism. Persistence in cell-free matrix with mineral particles would support the matrix mechanism. A sensitivity threshold is essential to interpret an absent signal.