ArticleJournal of bioenergetics and biomembranes2026
Mesenchymal stem cell-originated exosomal ZEB1 alleviates hypoxia/reperfusion-induced apoptosis, oxidative stress, and endoplasmic reticulum stress in cardiomyocytes via regulating UBIAD1.
Article in Journal of bioenergetics and biomembranes, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute myocardial infarction (AMI) is a major cardiovascular disease. Exosomes from mesenchymal stem cells (MSCs) are known to ameliorate myocardial ischemia-reperfusion (I/R) injury, and aberrant expression of UbiA prenyltransferase domain-containing protein 1 (UBIAD1) is linked to cardiovascular pathologies. However, it remains unclear whether MSC-derived exosomes mediate myocardial I/R injury by regulating UBIAD1.
methodsMSCs were identified by flow cytometry and differentiation assays (Alizarin Red and Oil Red O). Exosomes were characterized by transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), western blot, and immunofluorescence. Differentially expressed genes were analyzed using bioinformatics analysis. An in vitro H/R damage model was established. Protein expression was examined by western blot. For function, the cell viability, lactate dehydrogenase (LDH), malonaldehyde (MDA), glutathione (GSH), and reactive oxygen species (ROS) levels were detected using corresponding assay kits. Cell apoptosis was examined using flow cytometry. Cross-analysis of the transcription factors predicting UBIAD1 in hTFtarget with highly expressed genes in GSE202991 was analyzed using a Venn diagram. Besides, the interaction between ZEB1 and UBIAD1 was predicted and verified via JASPAR database, chromatin immunoprecipitation assay (ChIP) and dual-luciferase reporter assays.
resultsUp-regulated UBIAD1 mitigated H/R-induced injury in AC16 cells. Conversely, silencing UBIAD1 abrogated MSC-Exo-induced action of mitigation on H/R-induced AC16 cell injury. ZEB1 could bond to UBIAD1. Moreover, exosomes derived from sh-ZEB1-transfected MSCs reduced H/R-induced apoptosis and oxidative stress in cardiomyocytes. Importantly, exosomal ZEB1 alleviated H/R‑induced apoptosis, oxidative stress, and endoplasmic reticulum stress (ERS) through increasing UBIAD1.
conclusionMSC-derived exosomal ZEB1 remits H/R-stimulated cardiomyocyte apoptosis, oxidative stress, and ERS via regulating UBIAD1.
Indexed as
Identifiers
41849074What Socratic 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 Socratic graph.