ArticleKorean circulation journal2025
Article in Korean circulation journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- Temporal Trends in Cardiogenic Shock Complicating Acute Myocardial Infarction in South Korea.Korean circulation journal · 2026Article
- Nonsense-Mediated mRNA Decay: Mechanisms and Recent Implications in Cardiovascular Diseases.Cells · 2025Review
- Illuminating the Protective Role of UPF1 in Myocardial Ischemia/Reperfusion Injury.Korean circulation journal · 2025Article
- Ubiquitination-mediated protein homeostasis in cardiovascular diseases: molecular mechanisms and therapeutic opportunities.American journal of cardiovascular disease · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectivesMyocardial ischemia/reperfusion injury (MIRI) is an important factor affecting therapeutic effect and prognosis of acute myocardial infarction. Here, the effects of up-frameshift 1 (UPF1) on cardiomyocyte apoptosis in MIRI were evaluated.
methodsH9C2 cells were cultured under hypoxia/reoxygenation (H/R) condition. The expression of UPF1, SMAD-specific E3 ubiquitin ligase 2 (SMURF2), forkhead box A2 (FOXA2), protease-activated receptor 4 (PAR4), Bax, and Cleaved caspase-3 was assessed utilizing reverse transcription quantitative polymerase chain reaction and western blot. Cell viability and apoptosis were measured by Cell Counting Kit-8 and flow cytometry. Infarct area was examined by tetrazolium chloride staining in myocardial ischemia/reperfusion (I/R) rat model. HE and immunohistochemistry staining evaluated myocardial injury and UPF1 expression, respectively. Terminal deoxynucleotidyl transferase mediated dUTP nick end-labeling staining tested apoptosis. RNA immunoprecipitation, chromatin immunoprecipitation and dual luciferase assay verified molecular interactions. FOXA2 ubiquitination was detected by immunoprecipitation assay. SMURF2 mRNA stability was tested by actinomycin D treatment.
resultsFOXA2 effectively suppressed cardiomyocyte apoptosis induced by H/R by inhibiting PAR4 at transcriptional level. Degradation of FOXA2 was facilitated through SMURF2-mediated ubiquitination. Increased expression of UPF1 resulted in a reduction of H/R-induced cardiomyocyte apoptosis, and improved myocardial dysfunction caused by I/R in vivo. UPF1 influenced the decay of SMURF2 mRNA, leading to a decrease in its expression. Through SMURF2/FOXA2/PAR4 axis, UPF1 effectively suppressed cardiomyocyte apoptosis triggered by H/R.
conclusionsBy suppressing SMURF2 mRNA stability, UPF1 upregulated FOXA2 expression to inhibit PAR4, leading to inhibition of apoptosis during MIRI, which provides new therapeutic targets for MIRI treatment.
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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.