Oxidative stress-induced decreased expression of FABP5 leads to mitochondrial damage and survival disorder of decidual stromal cells in women with recurrent spontaneous abortion

Our findings demonstrate that FABP5 downregulation compromises DSC survival by disrupting MRPL17-dependent mitochondrial function, thereby attenuating CXCL11/CXCR3 mediated trophoblast invasion and migration. This study unveils a novel FABP5/MRPL17/CXCL11/CXCR3 axis in RSA pathogenesis, highlighting FABP5 as a potential therapeutic target for pregnancy maintenance.