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Maternal Western Diet Programmes Bile Acid Dysregulation and Hepatic Fibrosis in Fetal and Juvenile Macaques.
Liver Int
February 2025
Department of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
Background And Aims: Maternal obesity increases the risk of the paediatric form of metabolic dysfunction-associated steatotic liver disease (MASLD), affecting up to 30% of youth, but the developmental origins remain poorly understood.
Methods: Using a Japanese macaque model, we investigated the impact of maternal Western-style diet (mWSD) or chow diet followed by postweaning WSD (pwWSD) or chow diet focusing on bile acid (BA) homeostasis and hepatic fibrosis in livers from third-trimester fetuses and 3-year-old juvenile offspring.
Results: Juveniles exposed to mWSD had increased hepatic collagen I/III content and stellate cell activation in portal regions.
Laminin-dystroglycan mediated ferroptosis in hemorrhagic shock and reperfusion induced-cognitive impairment through AMPK/Nrf2.
Free Radic Biol Med
January 2025
Department of Anesthesiology and Perioperative Medicine, the Second Affiliated Hospital of Anhui Medical University, Hefei City, Anhui Province, China; Key Laboratory of Anesthesiology and Perioperative Medicine of Anhui Higher Education Institutes, Anhui Medical University, Hefei City, Anhui Province, China; Institute of Brain Science and Brain-inspired Research, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China. Electronic address:
Hemorrhagic shock and reperfusion (HSR) is the main cause of death following trauma. Cognitive impairment may persist after successful resuscitation from hemorrhagic shock, but the mechanisms remain elusive. This study demonstrated the presence of ferroptosis in an in vitro model of oxygen-glucose deprivation and reoxygenation (OGD/R) in HT22 neurons, and also in a murine model of HSR using 3-month-old C57BL/6 mice.
View Article and Find Full Text PDFMelatonin protects aged oocytes from depalmitoylation-mediated quality reduction by promoting PPT1 degradation and antioxidation.
Redox Biol
January 2025
Department of Reproductive Medicine, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, 210002, China; State Key Laboratory of Reproductive Medicine and Offspring Health, Nanjing Medical University, Nanjing, Jiangsu, 211166, China; Department of Reproductive Medicine, Affiliated Jinling Hospital, The First School of Clinical Medicine, Southern Medical University, Nanjing, 210002, China. Electronic address:
Oocyte aging is closely related to a decline in female fertility, accompanied by increased reactive oxygen species levels and changes in protein posttranslational modifications. However, the role of protein palmitoylation in oocyte aging has not been investigated. In the present study, a new association between redox and palmitoylation in aging oocytes was found.
View Article and Find Full Text PDFDe Novo Pathogenic Variant Associated with Lethal Encephalocardiomyopathy-Case Report and Literature Review.
Int J Mol Sci
January 2025
Institute for Maternal and Child Health IRCCS Burlo Garofolo, Via dell'Istria, 65, 34137 Trieste, Italy.
Pathogenic variants in , encoding dynamin-like protein-1 (DRP1), cause a lethal encephalopathy. DRP1 defective function results in altered mitochondrial networks, characterized by elongated/spaghetti-like, highly interconnected mitochondria. We validated in yeast the pathogenicity of a de novo variant identified by whole exome sequencing performed more than 10 years after the patient's death.
View Article and Find Full Text PDFMaternal exposure to bisphenol A induces congenital heart disease through mitochondrial dysfunction.
FASEB J
January 2025
Key Laboratory of Birth Defects and Related Diseases of Women and Children of MOE, Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, Sichuan, China.
Congenital heart disease (CHD) represents a major birth defect associated with substantial morbidity and mortality. Although environmental factors are acknowledged as potential contributors to CHD, the underlying mechanisms remain poorly understood. Bisphenol A (BPA), a common endocrine disruptor, has attracted significant attention due to its widespread use and associated health risks.
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