NLRP6 is essential for TREM2-alleviated cardiac ischemia/ reperfusion injury via affecting PANoptosis - PubMed
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- #PANoptosis
- NLRP6 is essential for TREM2-alleviated cardiac ischemia/reperfusion injury by affecting PANoptosis.
- TREM2 deficiency exacerbates necroptosis and acute myocardial injury, while soluble TREM2 (sTREM2) administration mitigates these effects.
- NLRP6 protein expression peaks at 48 hours post-reperfusion during I/R injury.
- TREM2 regulates NLRP6 and HMGB1 by inhibiting TLR4/NF-κB activation, reducing PANoptosis in cardiomyocytes.
- Inhibiting NLRP6 or HMGB1 reverses the pro-death effects caused by TREM2 deficiency.
- Plasma levels of NLRP6, TREM2, and HMGB1 are elevated in acute myocardial infarction (AMI) patients.
- TREM2 acts as a negative regulator of myocardial PANoptosis via the HMGB1/TLR4/NF-κB/NLRP6 axis.
- Targeting the TREM2-NLRP6 pathway may offer therapeutic potential for cardiac I/R injury.