Fig. 2

Abnormal amino acid metabolism and miscarriage. A. In the endometrium, a decrease in various amino acids can lead to the accumulation of uncharged tRNA, which in turn activates the GCN2/eIF2α/transcriptional activation factor 4 (ATF4) pathway, thereby inhibiting protein synthesis and inducing autophagy. B. At the maternal–fetal interface, meconium macrophages can promote trophoblast cell apoptosis by activating the PRMT3/ADMA/NO pathway and decreasing the concentration of NO in the meconium. SGC707 can reverse. C. Vitamin D deficiency can increase homocysteine levels by decreasing CBS, while inducing increased NK cell cytotoxicity and promoting inflammatory immune responses at the maternal–fetal interface. GCN2 the general control nonderepressible 2, eIF2αK4 eukaryotic translation initiation factor 2α kinase 4, ATF4 transcription activation factor 4, PRMTs type I protein L-arginine methyltransferases, SGC707 PRMT3 inhibitor, ADMA asymmetric dimethylarginine, NOS nitric oxide synthase, NO nitric oxide, CBS cystathionine beta-synthase, VitB6 Vitamin B6, VitD Vitamin D