Similar observations related to the upregulation of the p38 pathway have been linked to defects in the placental structure, elevated inflammation, and an increased apoptosis of cells in the junctional zone of rodent placentas, as noted in preeclamptic rats stimulated with N(omega)-nitro-L-arginine methyl ester (L-NAME) to induce clinical symptoms of preeclampsia [67]. Here, MAPK1 is linked to preeclampsia.