ArticleProceedings of the National Academy of Sciences of the United States of America2017
UCP1 deficiency causes brown fat respiratory chain depletion and sensitizes mitochondria to calcium overload-induced dysfunction.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
103 citing papers in PubMed, 176 citations in OpenAlex.
- Adipocyte Myoglobin Is a Determinant of Energy Expenditure and a Potential Target to Limit Obesity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Macrophage-derived itaconate is a negative regulator of adipose tissue thermogenesis.Nature metabolism · 2026Article
- The pro-tumorigenic functions of cancer-associated adipocytes are dependent on the mitochondrial chaperone tumor necrosis factor receptor-associated protein 1.Signal transduction and targeted therapy · 2026Article
- UCP1-Dependent Thermogenic Adipose Tissue in Human Disease: Adipose-Centered Mechanisms, Biomarker Limitations, and Translational Perspectives.International journal of molecular sciences · 2026Review
- Synergistic Intervention for Obesity: Integrating Central Appetite Regulation and Peripheral Energy Expenditure.Current obesity reports · 2026Review
- Rewiring Adipocyte Plasticity: The Redox-Mitochondrial Axis as a Driver of Beige Fat Immunometabolism and Adipose Inflammation.Biomolecules · 2026Review
- Chronic cold exposure induces plasticity of mitochondrial calcium uptake in beige and brown fat of UCP1-deficient mice.bioRxiv : the preprint server for biology · 2026Article
- Purinergic adipocyte-macrophage crosstalk promotes degeneration of thermogenic brown adipose tissue.EMBO reports · 2025Article
- PPA1 Facilitates Thermogenesis in Brown and Beige Fat by Regulating the Mitochondrial Localization of FUS.Current medical science · 2025Article
- Brown adipose tissue activity impacts systemic lactate clearance in male mice.The Journal of physiology · 2025Article
- Article
- Molecular mechanisms of UCP1-independent thermogenesis: the role of futile cycles in energy dissipation.Journal of physiology and biochemistry · 2025Review
- Haem biosynthesis regulates BCAA catabolism and thermogenesis in brown adipose tissue.Nature metabolism · 2025Article
- The Futile Creatine Cycle powers UCP1-independent thermogenesis in classical BAT.Nature communications · 2025Article
- Article
- Thermogenesis and Energy Metabolism in Brown Adipose Tissue in Animals Experiencing Cold Stress.International journal of molecular sciences · 2025Review
- Identification of a distal enhancer of Ucp1 essential for thermogenesis and mitochondrial function in brown fat.Communications biology · 2025Article
- Emerging debates and resolutions in brown adipose tissue research.Cell metabolism · 2025Review
- Article
- Enhanced mitochondrial buffering prevents CaThe Journal of physiology · 2024Article
43 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
Abstract
Brown adipose tissue (BAT) mitochondria exhibit high oxidative capacity and abundant expression of both electron transport chain components and uncoupling protein 1 (UCP1). UCP1 dissipates the mitochondrial proton motive force (Δp) generated by the respiratory chain and increases thermogenesis. Here we find that in mice genetically lacking UCP1, cold-induced activation of metabolism triggers innate immune signaling and markers of cell death in BAT. Moreover, global proteomic analysis reveals that this cascade induced by UCP1 deletion is associated with a dramatic reduction in electron transport chain abundance. UCP1-deficient BAT mitochondria exhibit reduced mitochondrial calcium buffering capacity and are highly sensitive to mitochondrial permeability transition induced by reactive oxygen species (ROS) and calcium overload. This dysfunction depends on ROS production by reverse electron transport through mitochondrial complex I, and can be rescued by inhibition of electron transfer through complex I or pharmacologic depletion of ROS levels. Our findings indicate that the interscapular BAT of
Indexed as
Identifiers
What OpenQuestion holds
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.