Mast Cell-Derived CXCL4: A Key Mediator of Ferroptosis and Cardiac Damage in Septic Cardiomyopathy - PubMed
4 days ago
- #septic cardiomyopathy
- #CXCL4
- #ferroptosis
- Mast cell-derived CXCL4 is a key mediator in septic cardiomyopathy (SCM), contributing to ferroptosis and cardiac damage.
- SCM is a severe complication of sepsis with high mortality, and the role of CXCL4 and ferroptosis in its progression was investigated.
- In vivo studies showed elevated CXCL4 levels in SCM mice, linked to mast cell activation and degranulation, which were mitigated by inhibitors like Sodium Cromoglycate (CS).
- In vitro, CXCL4 induced macrophage ferroptosis and impaired phagocytic function, reversed by ferroptosis inhibitor Ferrostatin-1 (Fer-1).
- The STAT3/P53 signaling pathway was identified as a key mechanism through which CXCL4 promotes macrophage ferroptosis and exacerbates SCM.
- Targeting mast cell activation, CXCL4 release, or the STAT3/P53-ferroptosis axis could be potential therapeutic strategies for SCM.