Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Cytosolic citrate is imported from the mitochondria by SLC25A1, and from the extracellular milieu by SLC13A5. In the cytosol, citrate is used by ACLY to generate acetyl-CoA, which can then be exported to the endoplasmic reticulum (ER) by SLC33A1. Here, we report the generation of mice with systemic overexpression (sTg) of SLC25A1 or SLC13A5. Both animals displayed increased cytosolic levels of citrate and acetyl-CoA; however, SLC13A5 sTg mice developed a progeria-like phenotype with premature death, while SLC25A1 sTg mice did not. Analysis of the metabolic profile revealed widespread differences. Furthermore, SLC13A5 sTg mice displayed increased engagement of the ER acetylation machinery through SLC33A1, while SLC25A1 sTg mice did not. In conclusion, our findings point to different biological responses to SLC13A5- or SLC25A1-mediated import of citrate and suggest that the directionality of the citrate/acetyl-CoA pathway can transduce different signals.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10492862 | PMC |
| http://dx.doi.org/10.1038/s42003-023-05311-1 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Inhaling Eugenol Inhibits NAFLD by Activating the Hepatic Ectopic Olfactory Receptor Olfr544 and Modulating the Gut Microbiota.
Adv Sci (Weinh)
August 2025
Academy of Chinese Medicine Sciences, Henan University of Chinese Medicine, Zhengzhou, 450046, China.
Non-alcoholic fatty liver disease (NAFLD) is a major public health threat with currently limited therapeutic options. Inhalation therapy shows promise for treating metabolic disorders due to rapid absorption and high patient adherence, though relevant medications remain scarce. Eugenol (EUG), the primary component of Syzygium aromaticum volatile oil, emerges as a promising NAFLD inhibitor from lipid-lowering aromatic Chinese medicine screening.
View Article and Find Full Text PDFGPX4 is a key ferroptosis regulator orchestrating T cells and CAR-T-cells sensitivity to ferroptosis.
Cancer Immunol Immunother
August 2025
Department of Immunology, Mossakowski Medical Research Institute Polish Academy of Sciences, 5 Adolfa Pawinskiego St., 02-106, Warsaw, Poland.
Induction of ferroptosis, an iron-dependent form of regulated cell death, holds promise as a strategy to overcome tumor resistance to conventional therapies and enhance immunotherapy responses. However, while the susceptibility of tumor cells to ferroptosis is extensively studied, limited data exists on the vulnerability of immune cells to disturbed iron balance and lipid peroxidation. Here, we found that T-cell stimulation rewires iron and redox homeostasis and by increasing levels of reactive oxygen species and labile iron promotes lipid peroxidation and T-cells' ferroptosis.
View Article and Find Full Text PDFSTING Agonist-Loaded Physalis Mottle Virus-like Particles as a Potent Prophylactic for Metastatic Melanoma.
ACS Appl Mater Interfaces
August 2025
Aiiso Yufeng Li Family Department of Chemical and Nano Engineering, University of California, San Diego, 9500 Gilman Dr., La Jolla, California 92093, United States.
Stimulator of interferon genes (STING) agonists have been presented as a compelling cancer therapeutic for many years yet have been unable to break past clinical trials. To date, the best use cases for STING agonists are as intratumoral therapeutics for solid tumors, but in human trials, rapid wash-out and low efficacy hamper success. Systemic administrations of STING agonists have also been explored, but hurdles include enzymatic instability, leading to rapid clearance and immune toxicity.
View Article and Find Full Text PDFAutocrine interferon poisoning mediates ADAR1-dependent synthetic lethality in BRCA1/2-mutant cancers.
Nat Commun
July 2025
The ERC (Epi)Genetic Vulnerabilities in Solid Tumors and Sarcoma Laboratory, Inserm Unit UMR981, Gustave Roussy, Villejuif, France.
ADAR1 is an RNA editing enzyme which prevents autoimmunity by blocking interferon responses triggered by cytosolic RNA sensors, and is a potential target in immuno-oncology. However, predictive biomarkers for ADAR1 inhibition are lacking. Using multiple in vitro and in vivo systems, we show that BRCA1/2 and ADAR1 are synthetically lethal, and that ADAR1 activity is upregulated in BRCA1/2-mutant cancers.
View Article and Find Full Text PDFMaternal emulsifier consumption alters the offspring early-life microbiota and goblet cell function leading to long-lasting diseases susceptibility.
Nat Commun
July 2025
Microbiome-Host Interactions, Institut Pasteur, Université Paris Cité, INSERM U1306, Paris, France.
Early-life acquisition of microbiota and, consequently, immune system development, both lastingly impacts health. Accordingly, we hypothesized that disturbing the microbiota of lactating mothers via consumption of dietary emulsifiers might alter the microbiota, and perhaps the immune system, of their offspring, thereby increasing susceptibility to microbiota-mediated diseases, including colitis and metabolic syndrome. Here we report that, in mice, maternal consumption of carboxymethylcellulose and polysorbate-80 resulted in transient alterations in offspring microbiotas that were necessary and sufficient to increase proneness to colitis and metabolic syndrome in young adulthood.
View Article and Find Full Text PDF