ArticleCell death discovery2022
Endogenous ROS production in early differentiation state suppresses endoderm differentiation via transient FOXC1 expression.
Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
The trial behind it
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Roles of Autophagy and Oxidative Stress in Cardiovascular Disease.Antioxidants (Basel, Switzerland) · 2025Review
- Understanding the mechanisms of mitochondrial rewiring during viral infections.The Journal of general virology · 2025Review
- Mitochondria and pluripotency: from established models to emerging roles in adult stem cells.Frontiers in bioengineering and biotechnology · 2025Review
- CKLF1, transcriptionally activated by FOXC1, promotes hypoxia/reoxygenation‑induced oxidative stress and inflammation in H9c2 cells by NLRP3 inflammasome activation.Experimental and therapeutic medicine · 2024Article
- ROS production by mitochondria: function or dysfunction?Oncogene · 2024Review
- Mitochondrial quality control: a pathophysiological mechanism and potential therapeutic target for chronic obstructive pulmonary disease.Frontiers in pharmacology · 2024Review
- Targeting Oxidative Stress with Polyphenols to Fight Liver Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- Potential antioxidative and anti-hyperuricemic components inFrontiers in pharmacology · 2023Article
- Nanopatterned bioresorbable elastomeric scaffolds to promote neural, glial, and endothelial differentiation using human embryonic and induced pluripotent stem cells.Journal of tissue engineeringArticle
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress plays a pivotal role in the differentiation and proliferation of cells and programmed cell death. However, studies on the role of oxidative stress in differentiation have mainly employed the detection of reactive oxygen species (ROS) during differentiation or generated by ROS inducers. Therefore, it is difficult to clarify the significance of endogenous ROS production in the differentiation of human cells. We developed a system to control the intracellular level of ROS in the initial stage of differentiation in human iPS cells. By introducing a specific substitution (I69E) into the SDHC protein, a component of the mitochondrial respiratory chain complex, the endogenous ROS level increased. This caused impaired endoderm differentiation of iPS cells, and this impairment was reversed by overproduction of mitochondrial-targeted catalase, an anti-oxidant enzyme. Expression of tumor-related FOXC1 transcription factor increased transiently as early as 4 h after ROS-overproduction in the initial stage of differentiation. Knockdown of FOXC1 markedly improved impaired endoderm differentiation, suggesting that endogenous ROS production in the early differentiation state suppresses endoderm differentiation via transient FOXC1 expression.
Identifiers
What OpenQuestion holds
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.