Cell death mechanisms in heat stroke and sepsis: ZBP1 and caspase-11 as molecular sensors driving the MLKL/GSDMD death execution axis - PubMed
3 hours ago
- #cell death
- #heat stroke
- #sepsis
- Heat stroke and sepsis are acute critical illnesses with similar outcomes despite different causes.
- Both conditions have high mortality rates and cause extensive organ damage.
- Necroptosis via ZBP1-RIPK3-MLKL and pyroptosis via caspase-11-GSDMD are key mechanisms in heat stroke and sepsis, respectively.
- ZBP1 senses heat stress, while caspase-11 responds to LPS, both leading to cell death.
- MLKL and GSDMD execute membrane-breaching mechanisms, driving organ damage.
- Targeting common downstream cell death pathways may offer new therapeutic strategies.