Nature Neuroscience, Journal Year: 2022, Volume and Issue: 25(7), P. 865 - 875
Published: June 20, 2022
Language: Английский
Nature Neuroscience, Journal Year: 2022, Volume and Issue: 25(7), P. 865 - 875
Published: June 20, 2022
Language: Английский
Science Advances, Journal Year: 2025, Volume and Issue: 11(4)
Published: Jan. 22, 2025
Birth is one of the most important life events for animals. However, its significance in developmental process not fully understood. Here, we found that birth-induced alteration glutamine metabolism radial glia (RG), embryonic neural stem cells (NSCs), required acquisition quiescence and long-term maintenance postnatal NSCs. Preterm birth impairs this cellular process, leading to transient hyperactivation RG. Consequently, brain, NSC pool depleted neurogenesis decreased. We also quiescent RG after preterm improves neurogenesis. This study demonstrates
Language: Английский
Citations
2Nature Communications, Journal Year: 2021, Volume and Issue: 12(1)
Published: March 26, 2021
Abstract Leigh syndrome (LS) is a severe manifestation of mitochondrial disease in children and currently incurable. The lack effective models hampers our understanding the mechanisms underlying neuronal pathology LS. Using patient-derived induced pluripotent stem cells CRISPR/Cas9 engineering, we developed human model LS caused by mutations complex IV assembly gene SURF1 . Single-cell RNA-sequencing multi-omics analysis revealed compromised morphogenesis mutant neural cultures brain organoids. defects emerged at level progenitor (NPCs), which retained glycolytic proliferative state that failed to instruct morphogenesis. NPCs carrying I NDUFS4 recapitulated defects. augmentation PGC1A induction via bezafibrate treatment supported metabolic programming NPCs, leading restored Our findings provide mechanistic insights suggest potential interventional strategies for rare disease.
Language: Английский
Citations
101Cell Reports, Journal Year: 2021, Volume and Issue: 35(2), P. 108952 - 108952
Published: April 1, 2021
The mechanisms controlling the post-natal maturation of astrocytes play a crucial role in ensuring correct synaptogenesis. We show that mitochondrial biogenesis developing is necessary for coordinating astrocyte and astrocytic depends on transient upregulation metabolic regulator peroxisome proliferator-activated receptor gamma (PPARγ) co-activator 1α (PGC-1α), which controlled by metabotropic glutamate 5 (mGluR5). At tissue level, loss or downregulation PGC-1α sustains proliferation, dampens morphogenesis, impairs formation function neighboring synapses, whereas its genetic re-expression sufficient to restore mitochondria compartment astroglial synaptic defects. Our findings developmental enhancement critical mechanism supporting synaptogenesis, thus suggesting may be therapeutic target case neurodevelopmental psychiatric disorders characterized impaired
Language: Английский
Citations
88Biomedicine & Pharmacotherapy, Journal Year: 2021, Volume and Issue: 137, P. 111327 - 111327
Published: Feb. 5, 2021
Increased life expectancies have significantly increased the number of individuals suffering from geriatric neurodegenerative diseases such as Alzheimer's disease (AD) and Parkinson's (PD). The financial cost for current future patients with these is overwhelming, resulting in substantial economic societal costs. Unfortunately, most recent high-profile clinical trials failed to obtain efficacious results, indicating that novel approaches are desperately needed treat pathologies. Cell senescence, characterized by permanent cell cycle arrest, resistance apoptosis, mitochondrial alterations, secretion senescence-associated secretory phenotype (SASP) components, has been extensively studied mitotic cells fibroblasts, which considered a hallmark aging. Furthermore, multiple types senescent state brain, including neurons, microglia, astrocytes, neural stem cells, recently observed context diseases, suggesting may play an essential role pathological processes diseases. Therefore, this review begins outlining key aspects senescence constitution followed examining evidence implicating In final section, we how be targeted therapeutics pathologies associated
Language: Английский
Citations
82Trends in Cell Biology, Journal Year: 2020, Volume and Issue: 30(3), P. 201 - 212
Published: Jan. 23, 2020
Language: Английский
Citations
78Cellular and Molecular Life Sciences, Journal Year: 2020, Volume and Issue: 77(13), P. 2483 - 2496
Published: Jan. 7, 2020
Abstract Understanding the mechanisms behind neurodifferentiation in adults will be an important milestone our quest to identify treatment strategies for cognitive disorders observed during natural ageing or disease. It is now clear that maturation of neural stem cells neurones, fully integrated into neuronal circuits requires a complete remodelling cellular metabolism, including switching energy source. Mitochondria are central this transition and increasingly seen as regulatory hub defining cell fate neurodevelopment. This review explores current knowledge metabolism adult neurodifferentiation.
Language: Английский
Citations
71Molecular Plant, Journal Year: 2022, Volume and Issue: 15(6), P. 943 - 955
Published: April 5, 2022
Language: Английский
Citations
66Cells, Journal Year: 2021, Volume and Issue: 11(1), P. 110 - 110
Published: Dec. 30, 2021
Environmental factors including diet, sedentary lifestyle and exposure to pollutants largely influence human health throughout life. Cellular molecular events triggered by an environmental are extremely variable depend on the age, chronicity doses of exposure. Only a fraction all relevant mechanisms involved in onset progression pathologies response toxicants has probably been identified. Mitochondria central hubs metabolic cell signaling responsible for large variety biochemical processes, oxidative stress, metabolite production, energy transduction, hormone synthesis, apoptosis. Growing evidence highlights mitochondrial dysfunction as major hallmark insults. Here, we present mitochondria crucial organelles healthy homeostasis whose induces critical adverse effects. Then, review multiple action causing toxicity link with chronic diseases. We propose Aryl hydrocarbon Receptor (AhR) model “exposome receptor”, activation leads various toxic through dysfunction. Finally, provide some remarks related mitotoxicity risk assessment.
Language: Английский
Citations
63Molecular Neurobiology, Journal Year: 2021, Volume and Issue: 58(5), P. 2342 - 2361
Published: Jan. 8, 2021
Language: Английский
Citations
62Cellular and Molecular Life Sciences, Journal Year: 2022, Volume and Issue: 79(5)
Published: April 13, 2022
Language: Английский
Citations
58