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Related Experiment Video

Updated: Jun 27, 2025

A Primary Human Trophoblast Model to Study the Effect of Inflammation Associated with Maternal Obesity on Regulation of Autophagy in the Placenta

A Primary Human Trophoblast Model to Study the Effect of Inflammation Associated with Maternal Obesity on Regulation of Autophagy in the Placenta

Published on: September 27, 2017

NBR1-dependent autophagy activation protects against environmental cadmium-evoked placental trophoblast senescence.

Qing Ling¹, Yu-Feng Zhang², Wei Chang¹

¹Department of Toxicology, School of Public Health, Anhui Medical University, China; Key Laboratory of Environmental Toxicology of Anhui Higher Education Institutes, China.

|April 26, 2024

Summary

This summary is machine-generated.

Environmental cadmium exposure induces placental cell senescence and autophagy. Activating autophagy protects against cadmium-induced placental aging, offering new strategies for developmental diseases.

Keywords:

Autophagy Cadmium NBR1 Placenta Senescence

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Quantifying Tissue-Specific Proteostatic Decline in Caenorhabditis elegans

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Published on: September 7, 2021

Area of Science:

Environmental Toxicology
Reproductive Biology
Cellular Senescence

Background:

Cadmium (Cd) is a developmental toxicant that accumulates in the placenta, impairing its function.
Environmental Cd exposure is linked to adverse pregnancy outcomes and placental cell senescence.
The role of autophagy in Cd-induced placental senescence remains unclear.

Purpose of the Study:

To investigate the role of autophagy activation in cadmium-induced placental cell senescence.
To elucidate the underlying mechanisms of this process.
To explore potential therapeutic strategies for mitigating Cd-induced placental damage.

Main Methods:

Animal experiments and cell culture models were used to study Cd exposure effects.
Pharmacological and genetic interventions were employed to modulate autophagy.
Case-control studies analyzed placental samples from pregnancies with fetal growth restriction.

Main Results:

Cadmium exposure during gestation induced placental senescence and activated autophagy.
Suppression of autophagy worsened Cd-induced placental senescence, while activation ameliorated it.
NBR1 knockdown exacerbated senescence; NBR1 facilitates p21 degradation via LC3B.

Conclusions:

Autophagy activation plays a protective role against cadmium-induced placental senescence.
NBR1-mediated degradation of p21 is a key mechanism in this process.
Findings suggest novel approaches for managing placental aging and related developmental disorders.