ArticleCell cycle (Georgetown, Tex.)2014
Tauroursodeoxycholic acid increases neural stem cell pool and neuronal conversion by regulating mitochondria-cell cycle retrograde signaling.
Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- Harnessing Endogenous Neural Stem Cells: A New Frontier in Spinal Cord Injury Repair.Neurochemical research · 2026Review
- Tauroursodeoxycholic acid reduces brain lesion volume and cortical edema in a rat model of Traumatic brain injury.Brain research · 2025Article
- Research Progress on the Mechanism of Bile Acids and Their Receptors in Depression.International journal of molecular sciences · 2025Review
- Ursodeoxycholic acid prompts glycolytic dominance, reductive stress and epithelial-to-mesenchymal transition in ovarian cancer cells through NRF2 activation.Cell death discovery · 2025Article
- Roles of bile acids signaling in neuromodulation under physiological and pathological conditions.Cell & bioscience · 2023Review
- Gut brain interaction theory reveals gut microbiota mediated neurogenesis and traditional Chinese medicine research strategies.Frontiers in cellular and infection microbiology · 2022Review
- Article
- Oxidative-Signaling in Neural Stem Cell-Mediated Plasticity: Implications for Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2021Review
- Neurotoxicity of mercury: an old issue with contemporary significance.Advances in neurotoxicology · 2021Article
- Mechanisms and rejuvenation strategies for aged hematopoietic stem cells.Journal of hematology & oncology · 2020Review
- Reprogramming of Lipid Metabolism as a New Driving Force Behind Tauroursodeoxycholic Acid-Induced Neural Stem Cell Proliferation.Frontiers in cell and developmental biology · 2020Article
- Amyloid β Peptide Compromises Neural Stem Cell Fate by Irreversibly Disturbing Mitochondrial Oxidative State and Blocking Mitochondrial Biogenesis and Dynamics.Molecular neurobiology · 2019Article
- Tauroursodeoxycholic Acid Enhances Mitochondrial Biogenesis, Neural Stem Cell Pool, and Early Neurogenesis in Adult Rats.Molecular neurobiology · 2018Article
- The role of mitochondria in stem cell fate and aging.Development (Cambridge, England) · 2018Review
- Article
- Oxidative stress response in neural stem cells exposed to different superparamagnetic iron oxide nanoparticles.International journal of nanomedicine · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The low survival and differentiation rates of stem cells after either transplantation or neural injury have been a major concern of stem cell-based therapy. Thus, further understanding long-term survival and differentiation of stem cells may uncover new targets for discovery and development of novel therapeutic approaches. We have previously described the impact of mitochondrial apoptosis-related events in modulating neural stem cell (NSC) fate. In addition, the endogenous bile acid, tauroursodeoxycholic acid (TUDCA) was shown to be neuroprotective in several animal models of neurodegenerative disorders by acting as an anti-apoptotic and anti-oxidant molecule at the mitochondrial level. Here, we hypothesize that TUDCA might also play a role on NSC fate decision. We found that TUDCA prevents mitochondrial apoptotic events typical of early-stage mouse NSC differentiation, preserves mitochondrial integrity and function, while enhancing self-renewal potential and accelerating cell cycle exit of NSCs. Interestingly, TUDCA prevention of mitochondrial alterations interfered with NSC differentiation potential by favoring neuronal rather than astroglial conversion. Finally, inhibition of mitochondrial reactive oxygen species (mtROS) scavenger and adenosine triphosphate (ATP) synthase revealed that the effect of TUDCA is dependent on mtROS and ATP regulation levels. Collectively, these data underline the importance of mitochondrial stress control of NSC fate decision and support a new role for TUDCA in this process.
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Registered trials
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