Defective Uteroplacental Vascular Remodeling in Preeclampsia: Key Molecular Factors Leading to Long Term Cardiovascular Disease (2021)
Kirim Hong, S. Kim, D. Cha, H. Park
Figure 1. Two step model of preeclampsia.
Figure 2. (a) Normal placentation with successful spiral artery remodeling. Endovascular trophoblasts become incorporated into the vessel wall and a fibrinoid layer substitutes the original smooth muscle cell layer, resulting in a low resistance vessel with a newly built thin, flexible wall which brings adequate uteroplacental perfusion. (b) Abnormal spiral artery remodeling in preeclampsia. Failure of endovascular trophoblast invasion results in a relatively narrow, thick-walled tortuous ve sel with high resistance leading to reduced uteroplacental perfusion (RUPP). Atherosis is shown with lipid deposition in wa ls of spiral arteries with lipid-fi led foam ce ls, perivascular lymphocytic infiltration and vascular fibrinoid necrosis.
https://pubmed.ncbi.nlm.nih.gov/31756606/
Defective Uteroplacental Vascular Remodeling in Preeclampsia: Key Molecular Factors Leading to Long Term Cardiovascular Disease (2021)
Kirim Hong, S. Kim, D. Cha, H. Park
Figure 1. Two step model of preeclampsia.
Figure 2. (a) Normal placentation with successful spiral artery remodeling. Endovascular trophoblasts become incorporated into the vessel wall and a fibrinoid layer substitutes the original smooth muscle cell layer, resulting in a low resistance vessel with a newly built thin, flexible wall which brings adequate uteroplacental perfusion. (b) Abnormal spiral artery remodeling in preeclampsia. Failure of endovascular trophoblast invasion results in a relatively narrow, thick-walled tortuous ve sel with high resistance leading to reduced uteroplacental perfusion (RUPP). Atherosis is shown with lipid deposition in wa ls of spiral arteries with lipid-fi led foam ce ls, perivascular lymphocytic infiltration and vascular fibrinoid necrosis.
https://pubmed.ncbi.nlm.nih.gov/31756606/