Abstract

Necroptosis is a form of newly defined programmed cell death. The fundamental characteristic of necroptotic cell death is the loss of membrane integrity and the release of intracellular contents. The necroptosis cell-released factors, so-called damage-associated molecular patterns (DAMPs), have drawn the most attention of researchers to study their pro-inflammatory roles in the past decades. Uncontrolled necroptosis leads to inflammatory injuries. However, whether necroptosis has any beneficial effect under physiological conditions is entirely unknown. Combining mouse genetics with techniques of molecular biology, cell biology, and biochemistry, we are dedicated to investigating the ‘beneficial roles’ of necroptosis in the context of tissue regeneration, which has been largely neglected for long; and to deciphering the molecular regulations of necroptosis signaling that balances cell survival or aberrant cell division.

Our recent study unveiled a hitherto uncharacterized “altruistic physiological role” of necroptosis promoting tissue regeneration. We also identified multi-levels of necroptosis-inhibitory regulations on the key necroptosis components RIP3 and MLKL, which explained how cells/organisms are protected from spontaneous necroptosis injury.