Abstract:  Programmed  cell  death  is  a  biological  process  regulated  by  molecular  mechanisms.  Apoptosis， necroptosis， and  pyroptosis  are  three  modalities  of  programmed  cell  death.  In  these  processes，  caspases  play  a  key regulatory role. Upon exposure to external stimuli or internal stressors， caspase-3/ 7 is activated by upstream caspase-8/ 9. This cascade  orchestrates  the  execution  of  apoptosis.  If  caspase-8  is  inhibited，  it  leads  to  the  activation  of  receptor- interacting protein kinase 3 （RIPK3）， which in turn phosphorylates  mixed lineage  kinase  domain-like  protein （MLKL）， triggering its oligomerization and subsequent membrane permeabilization， resulting in necroptosis. caspase-1/ 4/5/11 induce pyroptosis  by  cleaving  Gasdermin  family  molecules.  Furthermore，  the  oxidation  of  polyunsaturated  fatty  acids  within membrane  phospholipids  can  initiate  ferroptosis，  a  distinct  caspase-independent  pathway  of  cell  demise.  This  review summarizes  the   mechanisms   underlying   cell   death，   highlights   recent   research   advancements，   and   discusses   their implications for disease understanding.

Key words: programmed cell death ,  , caspase ,  , apoptosis ,  , necroptosis ,  ,  pyroptosis ,  ,  ferroptosis