Maternal one carbon metabolism through increased oxidative stress and disturbed angiogenesis can influence placental apoptosis in preeclampsia

Life Sciences
Vaishali V KastureSadhana R Joshi

Abstract

Adequate maternal nutrition is critical for a healthy pregnancy outcome and poor maternal nutrition is known to be associated with pregnancy complications like preeclampsia. We have earlier demonstrated that there is an imbalance in the levels of micronutrients (folate and vitamin B12) along with low levels of long chain polyunsaturated fatty acids (LCPUFA) and high homocysteine levels in women with preeclampsia. Homocysteine is known to be involved in the formation of free radicals leading to increased oxidative stress. Higher oxidative stress has been shown to be associated with increased apoptotic markers in the placenta. Preeclampsia is of placental origin and is associated with increased oxidative stress, disturbed angiogenesis and placental apoptosis. The process of angiogenesis is important for placental and fetal development and various angiogenic growth factors inhibit apoptosis by inactivation of proapoptotic proteins through a series of cellular signalling pathways. We propose that an altered one carbon cycle resulting in increased oxidative stress and impaired angiogenesis will contribute to increased placental apoptosis leading to preeclampsia. Understanding the association of one carbon cycle components and the po...Continue Reading

Citations

Nov 2, 2018·Clinical and Applied Thrombosis/hemostasis : Official Journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis·Mercedes de León BautistaAngélica Olivo-Díaz
Jun 7, 2020·Neurotoxicity Research·A D ShcherbitskaiaA V Arutjunyan
Mar 10, 2020·Food Science & Nutrition·Zhixiong MeiBenqi Teng
Dec 11, 2020·Differentiation; Research in Biological Diversity·R S SeelanM M Pisano
Jul 7, 2021·Biochemistry. Biokhimii︠a︡·Alexander V ArutjunyanIrina V Zalozniaia

❮ Previous
Next ❯

Related Concepts

Related Feeds

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis