ArticleCell and tissue research2026
Constitutive UCP1 expression is associated with a glucose-dependent phenotype in murine mesenchymal stem cells.
Article in Cell and tissue research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mesenchymal stem cells (MSCs) possess significant metabolic plasticity, enabling them to adapt dynamically to environmental stressors during tissue repair. Although UCP1 is associated with nonshivering thermogenesis in brown adipose tissue (BAT) through the uncoupling of oxidative phosphorylation, its impact on MSCs metabolism remains unexplored. Herein, we evaluated the ectopic expression of UCP1 in MSCs and its effects on classical surface markers, the redox state and glucose metabolism. MSCs were genetically modified to constitutively overexpress UCP1 using a lentiviral construct. Transduction efficiency was evaluated by direct UCP1 expression and the co-expressed EGFP fluorescent tag. Surface marker phenotype and proliferation were evaluated by expression of multipotency markers and metabolic activity, respectively. Metabolic phenotypes were assessed by measuring mitochondrial membrane potential (ΔΨm), quantifying cytoplasmic and mitochondrial reactive oxygen species (ROS), and evaluating glucose uptake via the 2-NBDG assay, while key glycolytic markers were evaluated by qPCR and immunoblot. UCP1-overexpressing MSCs showed a marked reduction in ΔΨm; however, normalized intracellular ATP levels remained stable across varying cell densities. Crucially, persistent UCP1 expression did not affect surface markers or cell metabolic activity, retaining their classical surface marker profile; furthermore, the engineered cells showed reduced baseline ROS levels compared with the parental line. Most notably, MSC-UCP1 cells showed increased glucose uptake and increased sensitivity to glucose deprivation, displaying increased expression of glycolytic markers. Our data indicate that constitutive UCP1 expression is associated with a shift in MSC metabolism towards a glucose-dependent state. This distinct metabolic profile highlights the plasticity of MSCs energetics and suggests a potential therapeutic application for genetically engineered MSCs in treating energy imbalance disorders such as obesity and type 2 diabetes.
Indexed as
Identifiers
42894040What 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.