ArticleAutophagy2013
Placental autophagy regulation by the BOK-MCL1 rheostat.
Article in Autophagy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
39 citing papers in PubMed, 64 citations in OpenAlex.
- Autophagy in PE: Dispute, Role and Potential Target.Cell proliferation · 2025Review
- Article
- Upregulation of Autophagy During the Differentiation of Primary Human Term Cytotrophoblast Cells into Syncytial Cells: Ultrastructural Analysis.International journal of molecular sciences · 2025Article
- Nutraceuticals in Pregnancy: A Special Focus on Probiotics.International journal of molecular sciences · 2024Review
- Inhibition of autophagy via 3-methyladenine alleviates the progression of preeclampsia.Acta biochimica et biophysica Sinica · 2024Article
- The regulated cell death at the maternal-fetal interface: beneficial or detrimental?Cell death discovery · 2024Review
- An integral role of mitochondrial function in the pathophysiology of preeclampsia.Molecular biology reports · 2024Review
- Mechanisms of BCL-2 family proteins in mitochondrial apoptosis.Nature reviews. Molecular cell biology · 2023Review
- Observation of increased levels of autophagy-related genes and proteins in women with preeclampsia: a clinical study.Molecular biology reports · 2023Article
- The Role of Autophagy in the Female Reproduction System: For Beginners to Experts in This Field.Biology · 2023Review
- The endoplasmic reticulum stress and B cell lymphoma-2 related ovarian killer participate in docosahexaenoic acid-induced adipocyte apoptosis in grass carp (Ctenopharyngodon idellus).Journal of animal science · 2023Article
- Understanding MCL1: from cellular function and regulation to pharmacological inhibition.The FEBS journal · 2022Review
- Dichotomy in hypoxia-induced mitochondrial fission in placental mesenchymal cells during development and preeclampsia: consequences for trophoblast mitochondrial homeostasis.Cell death & disease · 2022Article
- Insight of Autophagy in Spontaneous Miscarriage.International journal of biological sciences · 2022Review
- Impaired placental mitophagy and oxidative stress are associated with dysregulated BNIP3 in preeclampsia.Scientific reports · 2021Article
- CLDN1 regulates trophoblast apoptosis and proliferation in preeclampsia.Reproduction (Cambridge, England) · 2021Article
- Molecular and immunological developments in placentas.Human immunology · 2021Review
- BOK-MCL1 transmembrane interactions: a challenging target for cancer therapy.Molecular & cellular oncology · 2021Article
- Autophagy Process in Trophoblast Cells Invasion and Differentiation: Similitude and Differences With Cancer Cells.Frontiers in oncology · 2021Review
- Preeclampsia: From Cellular Wellness to Inappropriate Cell Death, and the Roles of Nutrition.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
Autophagy is the catabolic degradation of cellular cytoplasmic constituents via the lysosomal pathway that physiologically elicits a primarily cytoprotective function, but can rapidly be upregulated in response to stressors thereby inducing cell death. We have reported that the balance between the BCL2 family proteins BOK and MCL1 regulates human trophoblast cell fate and its alteration toward cell death typifies preeclampsia. Here we demonstrate that BOK is a potent inducer of autophagy as shown by increased LC3B-II production, autophagosomal formation and lysosomal activation in HEK 293. In contrast, using JEG3 cells we showed that prosurvival MCL1 acts as a repressor of autophagy via an interaction with BECN1, which is abrogated by BOK. We found that MCL1-cleaved products, specifically MCL1c157, trigger autophagy while the splicing variant MCL1S has no effect. Treatment of JEG3 cells with nitric oxide donor SNP resulted in BOK-MCL1 rheostat dysregulation, favoring BOK accumulation, thereby inducing autophagy. Overexpression of MCL1 rescued oxidative stress-induced autophagy. Of clinical relevance, we report aberrant autophagy levels in the preeclamptic placenta due to impaired recruitment of BECN1 to MCL1. Our data provided the first evidence for a key role of the BOK-MCL1 system in regulating autophagy in the human placenta, whereby an adverse environment as seen in preeclampsia tilts the BOK-MCL1 balance toward the build-up of isoforms that triggers placental autophagy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.