Dead-cell remnants sustain skin inflammation

This proposed skin hypothesis asks why inflammation and growth of the connective tissue beneath the epidermis can recur after the skin barrier has recovered, a question that matters for restoring more youthful function in middle-aged skin. It proposes that macrophages, immune cells that engulf and break down dead cells, may face a lingering queue: a small fraction of cellular fragments takes unusually long to process. That residual cargo could sustain inflammatory memory and dermal growth. A rival explanation places the memory in keratinocytes, the main epidermal cells, where extrachromosomal genetic material might persist. The test is direct: verify complete cargo removal while epidermal DNA and chromatin stay unchanged, then ask whether the recurrent response shortens.