We thought we found the enemy. At first, senescent cells, sometimes called “zombie cells,” looked like aging’s villains. They had stopped dividing but remained metabolically active, sending signals that could inflame or damage the tissue around them. In mice, eliminating these cells delayed or improved several age-related conditions, and in some experiments extended remaining lifespan. This raised an enticing possibility: perhaps killing senescent cells could make people live longer, healthier lives.
But then we realized a new problem: senescent cells are not a single, easily identified enemy. Not only are biomarkers and cellular proteins not consistently reliable, but the tissue…
