Hypoxia-ischemia and sexual dimorphism: modeling mitochondrial dysfunction using brain organoids
Abstract Hypoxic–ischemic encephalopathy (HIE) is a leading cause of neurodevelopmental morbidities in full-term infants. There is strong evidence of sexual differences in hypoxic-ischemic (HI) injury where male neonates are at higher risk as they are subject to more pronounced neurological deficits...
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| Language: | English |
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BMC
2025-05-01
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| Series: | Cell & Bioscience |
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| Online Access: | https://doi.org/10.1186/s13578-025-01402-0 |
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| author | Romane Gaston-Breton Clémence Disdier Henrik Hagberg Aloïse Mabondzo |
| author_facet | Romane Gaston-Breton Clémence Disdier Henrik Hagberg Aloïse Mabondzo |
| author_sort | Romane Gaston-Breton |
| collection | DOAJ |
| description | Abstract Hypoxic–ischemic encephalopathy (HIE) is a leading cause of neurodevelopmental morbidities in full-term infants. There is strong evidence of sexual differences in hypoxic-ischemic (HI) injury where male neonates are at higher risk as they are subject to more pronounced neurological deficits and death than females. The cellular and molecular mechanisms underlying these sexual discrepancies in HI injury are poorly understood. Mitochondrial dysregulation has been increasingly explored in brain diseases and represents a major target during HI events. In this review, we discuss (1) different mitochondrial functions in the central nervous system (2), mitochondrial dysregulation in the context of HI injury (3), sex-dependent mitochondrial pathways in HIE and (4) modeling of mitochondrial dysfunction using human brain organoids. Gaining insight into these novel aspects of mitochondrial function will offer valuable understanding of brain development and neurological disorders such as HI injury, paving the way for the discovery and creation of new treatment approaches. |
| format | Article |
| id | doaj-art-5ecb6b3a7ccf4f56b81df720d5e77d01 |
| institution | DOAJ |
| issn | 2045-3701 |
| language | English |
| publishDate | 2025-05-01 |
| publisher | BMC |
| record_format | Article |
| series | Cell & Bioscience |
| spelling | doaj-art-5ecb6b3a7ccf4f56b81df720d5e77d012025-08-20T03:08:44ZengBMCCell & Bioscience2045-37012025-05-0115111410.1186/s13578-025-01402-0Hypoxia-ischemia and sexual dimorphism: modeling mitochondrial dysfunction using brain organoidsRomane Gaston-Breton0Clémence Disdier1Henrik Hagberg2Aloïse Mabondzo3Université Paris-Saclay, CEA, INRAE, Département Médicaments et Technologies pour la Santé (DMTS), SPI, Laboratoire d’Etude de l’Unité Neurovasculaire & Innovation Thérapeutique (LENIT)Université Paris-Saclay, CEA, INRAE, Département Médicaments et Technologies pour la Santé (DMTS), SPI, Laboratoire d’Etude de l’Unité Neurovasculaire & Innovation Thérapeutique (LENIT)Perinatal Center, Sahlgrenska AcademyUniversité Paris-Saclay, CEA, INRAE, Département Médicaments et Technologies pour la Santé (DMTS), SPI, Laboratoire d’Etude de l’Unité Neurovasculaire & Innovation Thérapeutique (LENIT)Abstract Hypoxic–ischemic encephalopathy (HIE) is a leading cause of neurodevelopmental morbidities in full-term infants. There is strong evidence of sexual differences in hypoxic-ischemic (HI) injury where male neonates are at higher risk as they are subject to more pronounced neurological deficits and death than females. The cellular and molecular mechanisms underlying these sexual discrepancies in HI injury are poorly understood. Mitochondrial dysregulation has been increasingly explored in brain diseases and represents a major target during HI events. In this review, we discuss (1) different mitochondrial functions in the central nervous system (2), mitochondrial dysregulation in the context of HI injury (3), sex-dependent mitochondrial pathways in HIE and (4) modeling of mitochondrial dysfunction using human brain organoids. Gaining insight into these novel aspects of mitochondrial function will offer valuable understanding of brain development and neurological disorders such as HI injury, paving the way for the discovery and creation of new treatment approaches.https://doi.org/10.1186/s13578-025-01402-0MitochondriaHypoxic-ischemic encephalopathySexual differencesBrain organoid |
| spellingShingle | Romane Gaston-Breton Clémence Disdier Henrik Hagberg Aloïse Mabondzo Hypoxia-ischemia and sexual dimorphism: modeling mitochondrial dysfunction using brain organoids Cell & Bioscience Mitochondria Hypoxic-ischemic encephalopathy Sexual differences Brain organoid |
| title | Hypoxia-ischemia and sexual dimorphism: modeling mitochondrial dysfunction using brain organoids |
| title_full | Hypoxia-ischemia and sexual dimorphism: modeling mitochondrial dysfunction using brain organoids |
| title_fullStr | Hypoxia-ischemia and sexual dimorphism: modeling mitochondrial dysfunction using brain organoids |
| title_full_unstemmed | Hypoxia-ischemia and sexual dimorphism: modeling mitochondrial dysfunction using brain organoids |
| title_short | Hypoxia-ischemia and sexual dimorphism: modeling mitochondrial dysfunction using brain organoids |
| title_sort | hypoxia ischemia and sexual dimorphism modeling mitochondrial dysfunction using brain organoids |
| topic | Mitochondria Hypoxic-ischemic encephalopathy Sexual differences Brain organoid |
| url | https://doi.org/10.1186/s13578-025-01402-0 |
| work_keys_str_mv | AT romanegastonbreton hypoxiaischemiaandsexualdimorphismmodelingmitochondrialdysfunctionusingbrainorganoids AT clemencedisdier hypoxiaischemiaandsexualdimorphismmodelingmitochondrialdysfunctionusingbrainorganoids AT henrikhagberg hypoxiaischemiaandsexualdimorphismmodelingmitochondrialdysfunctionusingbrainorganoids AT aloisemabondzo hypoxiaischemiaandsexualdimorphismmodelingmitochondrialdysfunctionusingbrainorganoids |