Cilium loss prolongs skin proliferation

This proposed mechanism asks if shifted sleep schedules could prolong repair in reconstructed skin. It centres on fibroblasts, dermal support cells, whose clock phases may be clustered or spread out. The test matches timing, clock amplitude, cell mix, injury and treatment. It measures how long primary cilia, signal-sensing cell projections, disappear together, and whether cells return to division before the next cycle. It predicts that spread-out phases retain a scatter of reassembled cilia, restraining renewed proliferation. Inducing cilium reassembly after initial migration would test it. Alternatively, variable weak inflammatory input could drive repeated nuclear factor kappa B, an inflammatory signal, and residual proliferation. Both mechanisms could contribute.