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Cancer progression is tightly linked to metabolic changes, particularly in lipid metabolism, which is crucial for tumor growth and metastasis. Exercise, known for its health benefits, is gaining recognition for its ability to influence cancer-related lipid metabolism. Metabolic shift prioritizes lipid oxidation over glucose metabolism, hence limiting the energy supply available to tumor cells and reducing their metabolic adaptability. Exercise also enhances mitochondrial function and aids the immune system, further bolstering its anti-cancer effects. Additionally, exercise mitigates cancer-related symptoms like fatigue, improves insulin sensitivity, and counteracts metabolic issues such as cachexia. Despite promising insights from studies, challenges persist in comprehending the molecular mechanisms of exercise's impact on lipid metabolism in cancer. Future research should aim to identify optimal exercise regimens for cancer patients, explore the combined effects of exercise and cancer treatments, and delve into the molecular pathways connecting exercise with tumor suppression. With its potential benefits, exercise could act as a supportive therapy alongside conventional cancer treatments, enhancing patient outcomes and quality of life.
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http://dx.doi.org/10.3389/fendo.2025.1580559 | DOI Listing |
Proc Natl Acad Sci U S A
September 2025
Institute for Complex Molecular Systems, Eindhoven University of Technology, Eindhoven 5600 MB, The Netherlands.
Multivalent binding and the resulting dynamical clustering of receptors and ligands are known to be key features in biological interactions. For optimizing biomaterials capable of similar dynamical features, it is essential to understand the first step of these interactions, namely the multivalent molecular recognition between ligands and cell receptors. Here, we present the reciprocal cooperation between dynamic ligands in supramolecular polymers and dynamic receptors in model cell membranes, determining molecular recognition and multivalent binding via receptor clustering.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
September 2025
Department of Neuroscience, The Scripps Research Institute, San Diego, CA 92037.
Microglia regulate neuronal circuit plasticity. Disrupting their homeostatic function has detrimental effects on neuronal circuit health. Neuroinflammation contributes to the onset and progression of neurodegenerative diseases, including Alzheimer's disease (AD), with several microglial activation genes linked to increased risk for these conditions.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
September 2025
State Key Laboratory of Membrane Biology, IDG/McGovern Institute for Brain Research, School of Life Sciences, Tsinghua University, Beijing 100084, China.
Although clinical research has revealed microglia-related inflammatory and immune responses in bipolar disorder (BD) patient brains, it remains unclear how microglia contribute to the pathogenesis of BD. Here, we demonstrated that Serinc2 is associated with susceptibility to BD and showed a reduced expression in BDII patient plasma, which correlated with the disease severity. Using induced pluripotent stem cell (iPSC) models of sporadic and familial BDII patients, we found that Serinc2 expression showed deficits in iPSC-derived microglia-like cells, resulting in decreased synaptic pruning.
View Article and Find Full Text PDFAm J Physiol Cell Physiol
September 2025
Institute of Pharmacology and Toxicology, Goethe University Frankfurt, Frankfurt, Germany.
The A20 binding inhibitor of nuclear factor-kappa B (NF-κB)-1 (ABIN-1) serves as a ubiquitin sensor and autophagy receptor, crucial for modulating inflammation and cell death. Our previous in vitro investigation identified the LC3-interacting region (LIR) motifs 1 and 2 of ABIN-1 as key mitophagy regulators. This study aimed to explore the in vivo biological significance of ABIN1-LIR domains using a novel CRISPR-engineered ABIN1-ΔLIR1/2 mouse model, which lacks both LIR motifs.
View Article and Find Full Text PDFJ Infect Dis
September 2025
Section of Infectious Diseases, Yale School of Medicine, New Haven, CT, USA.
Background: Women are disproportionately affected by neuropsychiatric symptoms following recovery from acute COVID-19. However, whether there are central nervous system-specific changes in gene expression in women with neuropsychiatric Long COVID (NP-Long COVID) remains unknown.
Methods: Twenty-two women with and ten women without NP-Long COVID were enrolled from New Haven, CT, and the surrounding region and consented to a blood draw and large volume lumbar puncture.