What is Regulated necrosis and senescence?

Cells have other programmed deaths, all inflammatory where apoptosis is silent. Necroptosis, triggered by death receptors when caspase-8 is blocked (as some viruses block it), assembles the kinase RIPK3 with MLKL, which punctures the plasma membrane. Pyroptosis, in infected macrophages, is executed by caspase-1 of the inflammasome (Chapter 15), which cleaves gasdermin into a pore-former and releases interleukin-1. Ferroptosis is death by iron-dependent lipid peroxidation. A cell can also stop dividing without dying: senescence is a permanent arrest, enforced by p16 and p21 after telomere erosion (Chapter 24), persistent DNA damage or oncogene activation, in which the cell stays metabolically active and secretes inflammatory factors. Senescence removes damaged cells from the dividing pool — a tumour suppressor — and accumulates with age, where its secretions contribute to the degeneration of tissues; clearing senescent cells in mice extends healthy life.