Autophagy in the placenta

Abstract

Autophagy is an evolutionarily conserved catalytic process by which cytoplasmic components including damaged macromolecules and organelles are degraded. The role of autophagy includes adaptive responses to nutrition deprivation or intracellular stimuli. Although autophagosomes were first observed in early 1960s, it was 1990s that autophagy-related genes in yeast were identified and studied. Nowadays, the molecular machinery of autophagy and signaling pathway to various stimuli are almost outlined. Dysregulation of autophagic activity has been implicated in many human diseases including neurodegenerative diseases, infection and inflammation, and malignancies. However, since current understanding of autophagy in placenta is just at the beginning, this paper aims to provide general information on autophagy (part I) and to summarize articles on autophagy in human placenta (part II). This review article will serve as a basis for further researches on autophagy in relation to human pregnancy and its complications.

Ozone-induced fetal growth restriction in rats is associated with sexually dimorphic placental and fetal metabolic adaptation

“…One such mechanism that the placenta may undertake to reduce its own cellular energy requirements is autophagy, which is known to be activated during times of stress (for example, hypoxia, changes in resource availability, and inflammatory injury) [ 42 ]. As a critical regulator of autophagy, AMPKα controls numerous cellular pathways that promote autophagosome development, reduce inflammatory signaling, and suppress protein synthesis.…”

“…In contrast to the high metabolic capacity and demand of the male placenta in the current study, autophagy markers were upregulated in the female placenta. Autophagy is a cellular defense mechanism that may serve to protect basal cellular function in the face of nutrient deprivation and/or during inflammatory stress [ 42 ]. Thus, predictably, elevated levels of autophagy have been observed in placentae from pregnancies complicated with preeclampsia and in rodent models of acute maternal food deprivation [ 42 , 49 ].…”

“…Autophagy is a cellular defense mechanism that may serve to protect basal cellular function in the face of nutrient deprivation and/or during inflammatory stress [ 42 ]. Thus, predictably, elevated levels of autophagy have been observed in placentae from pregnancies complicated with preeclampsia and in rodent models of acute maternal food deprivation [ 42 , 49 ]. While the role of autophagy remains an area of active investigation [ 50 ], placental-specific deletion of ATG7 has been shown to be associated with an elevated risk of cardiometabolic disease in male offspring [ 26 ].…”

Autophagy regulates trophoblast invasion by targeting NF-κB activity

“…Autophagy is understood as a mechanism for both cell death and cytoprotection depending on the cellular types and contexts, and it has been implicated in various physiological and pathological conditions 6 , 7 . Without exception, autophagy is also involved in numerous physiological and pathological processes of human reproduction and pregnancy complications 8 – 11 . Undue autophagic activity upon non-physiological stimuli such as excessive inflammation or severe oxidative stress may limit trophoblast invasion, resulting in defective placentation 12 .…”

Linc02527 promoted autophagy in Intrahepatic cholestasis of pregnancy

“…Autophagy is an evolutionarily conserved catalytic process by which cytoplasmic components including damaged macromolecules and organelles are degraded 43 . An increased autophagosome formation was observed in placenta from preeclampsia and FGR 44 . In this study, we found LC3-II expression was elevated in placenta from ICP.…”