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http://dx.doi.org/10.1074/jbc.A115.649657 | DOI Listing |
J Exp Clin Cancer Res
January 2025
Department of Thoracic Surgery, Shanghai Tongji Hospital Affiliated With Tongji University, Shanghai, 200065, P. R. China.
EMBO J
January 2025
Department of Immunology and Regenerative Biology, Weizmann Institute of Science, 76100, Rehovot, Israel.
Mitochondrial carrier homolog 2 (MTCH2) is a regulator of apoptosis, mitochondrial dynamics, and metabolism. Loss of MTCH2 results in mitochondrial fragmentation, an increase in whole-body energy utilization, and protection against diet-induced obesity. In this study, we used temporal metabolomics on HeLa cells to show that MTCH2 deletion results in a high ATP demand, an oxidized cellular environment, and elevated utilization of lipids, amino acids, and carbohydrates, accompanied by a decrease in several metabolites.
View Article and Find Full Text PDFEMBO Rep
January 2025
Department of Molecular and Medical Pharmacology, University of California, Los Angeles, Los Angeles, CA, USA.
Pro-inflammatory macrophage activation is a hallmark example of how mitochondria serve as signaling organelles. Oxidative phosphorylation sharply decreases upon classical macrophage activation, as mitochondria are thought to shift from ATP production towards accumulating signals that amplify effector function. However, evidence is conflicting regarding whether this collapse in respiration is essential or dispensable.
View Article and Find Full Text PDFRedox Biol
December 2024
Department of Anesthesiology, Tianjin Medical University General Hospital, Tianjin, 300052, China; Tianjin Research Institute of Anesthesiology, Tianjin, 300052, China. Electronic address:
Chronic itch which is primarily associated with dermatologic, systemic, or metabolic disorders is often refractory to most current antipruritic medications, thus highlighting the need for improved therapies. Oxidative damage is a novel determinant of spinal pruriceptive sensitization and synaptic plasticity. The resolution of oxidative insult by molecular hydrogen has been manifested.
View Article and Find Full Text PDFAquat Toxicol
December 2024
Key Laboratory of Tropical Marine Bio-resources and Ecology, Guangdong Provincial Key Laboratory of Applied Marine Biology, South China Sea Institute of Oceanology, Chinese Academy of Sciences, Guangzhou 510301, China; Sanya Institute of Ocean Eco-Environmental Engineering, Sanya 572025, China. Electronic address:
Arsenic (As) is widely recognized for its hazards to aquatic organisms; however, its toxicological impacts on apoptosis in marine fish remain inadequately explored. This study investigated the effects of in vivo dietary exposure to 50 or 500 mg/kg AsIII (as NaAsO) over 28 days in marine medaka, alongside in vitro exposure to 50-750 μg/L AsIII for 48 h in a hepatic cell line derived from marine medaka, to elucidate the toxicity and underlying molecular mechanisms. In vivo, As significantly accumulated in liver tissue (1.
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