ArticleProtein & cell2016
Homocysteine activates T cells by enhancing endoplasmic reticulum-mitochondria coupling and increasing mitochondrial respiration.
Article in Protein & cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed, 48 citations in OpenAlex.
- Metabolic adaptation to IMMT deficiency through the ATF6-PPARγ axis is contingent on TP53 mutation status in breast cancer.Cell death & disease · 2026Article
- The spatiotemporal dynamics of MAMs: mechanisms, pathologies, and therapeutic rewiring.Cellular & molecular biology letters · 2026Review
- Immune profiling in a living human recipient of a gene-edited pig kidney.Nature medicine · 2026Article
- Role of hyperhomocysteinemia in atherosclerosis: from bench to bedside.Annals of medicine · 2025Review
- Dysregulated homocysteine metabolism and cardiovascular disease and clinical treatments.Molecular and cellular biochemistry · 2025Review
- Pyruvate kinase M2 activation reprograms mitochondria in CD8 T cells, enhancing effector functions and efficacy of anti-PD1 therapy.Cell metabolism · 2025Article
- Endoplasmic reticulum-mitochondria crosstalk: new mechanisms in the development of atherosclerosis.Frontiers in endocrinology · 2025Review
- Homocysteine Promotes Intestinal Inflammation in Colitis Mice Through the PGE2/STAT3 Signaling Pathway.Digestive diseases and sciences · 2024Article
- S-adenosyl-L-methionine supplementation alleviates aortic dissection by decreasing inflammatory infiltration.Nutrition & metabolism · 2024Article
- Effects of Aerobic Treadmill Training on Oxidative Stress Parameters, Metabolic Enzymes, and Histomorphometric Changes in Colon of Rats with Experimentally Induced Hyperhomocysteinemia.International journal of molecular sciences · 2024Article
- The Role of Methionine Restriction in Gastric Cancer: A Summary of Mechanisms and a Discussion on Tumor Heterogeneity.Biomolecules · 2024Review
- Mitochondrial dysfunctions in T cells: focus on inflammatory bowel disease.Frontiers in immunology · 2023Review
- Bioinformatics analysis to screen for genes related to myocardial infarction.Frontiers in genetics · 2022Article
- Methionine cycle-dependent regulation of T cells in cancer immunity.Frontiers in oncology · 2022Review
- Review
- Dynamic regulation of mitochondrial-endoplasmic reticulum crosstalk during stem cell homeostasis and aging.Cell death & disease · 2021Review
- Innate-adaptive immunity interplay and redox regulation in immune response.Redox biology · 2020Review
- Hyperhomocysteinemia and Endothelial Dysfunction in Multiple Sclerosis.Brain sciences · 2020Article
- Role of Endoplasmic Reticulum Stress in Atherosclerosis and Its Potential as a Therapeutic Target.Oxidative medicine and cellular longevity · 2020Review
- Mitochondrial Contact Sites in Inflammation-Induced Cardiovascular Disease.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperhomocysteinemia (HHcy) accelerates atherosclerosis by increasing proliferation and stimulating cytokine secretion in T cells. However, whether homocysteine (Hcy)-mediated T cell activation is associated with metabolic reprogramming is unclear. Here, our in vivo and in vitro studies showed that Hcy-stimulated splenic T-cell activation in mice was accompanied by increased levels of mitochondrial reactive oxygen species (ROS) and calcium, mitochondrial mass and respiration. Inhibiting mitochondrial ROS production and calcium signals or blocking mitochondrial respiration largely blunted Hcy-induced T-cell interferon γ (IFN-γ) secretion and proliferation. Hcy also enhanced endoplasmic reticulum (ER) stress in T cells, and inhibition of ER stress with 4-phenylbutyric acid blocked Hcy-induced T-cell activation. Mechanistically, Hcy increased ER-mitochondria coupling, and uncoupling ER-mitochondria by the microtubule inhibitor nocodazole attenuated Hcy-stimulated mitochondrial reprogramming, IFN-γ secretion and proliferation in T cells, suggesting that juxtaposition of ER and mitochondria is required for Hcy-promoted mitochondrial function and T-cell activation. In conclusion, Hcy promotes T-cell activation by increasing ER-mitochondria coupling and regulating metabolic reprogramming.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.