ArticleAnnals of medicine and surgery (2012)2023
Ischemia-reperfusion injury in human AC16 cardiomyocytes is modulated by AXIN1 depending on c-Myc regulation.
Article in Annals of medicine and surgery (2012), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed, 22 citations in OpenAlex.
- Expression Profiling and Transcriptional Coordination of Canonical Wnt Signaling Pathway Genes (FZD2, DVL2, and AXIN1) in Chronic Venous Insufficiency.Biomedicines · 2026Article
- Kaempferol Attenuates Myocardial Ischemia-Reperfusion Injury by Suppressing Ferroptosis via the KEAP1-Nrf2-GPX4 Axis.The Kaohsiung journal of medical sciences · 2026Article
- MiR-200a-3p protects against myocardial ischemia-reperfusion injury via KEAP1-NRF2 signaling.Frontiers in physiology · 2026Article
- Hypoxic Small Extracellular Vesicle Preconditioning of AC16 Cardiomyocytes Increase Caspase-3 and Caspase-8 Activity During Hypoxia.International journal of molecular sciences · 2025Article
- Axin formation inhibitor 1 aggravates hepatic ischemia‒reperfusion injury by promoting the ubiquitination and degradation of PPARβ.Nature communications · 2025Article
- Exosomal Preconditioning of Human iPSC-Derived Cardiomyocytes Beneficially Alters Cardiac Electrophysiology and Micro RNA Expression.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: A major consequence of acute myocardial infarction is myocardial ischemia-reperfusion (I/R) injury. Collecting proof demonstrates that AXIN1 assume a basic part in different disease; however, the role of AXIN1 in I/R injury remains to a great extent obscure. Methods: The I/R injury model on AC16 cells was constructed. siRNA transfection was used to knockdown AXIN1. The qRT-PCR assays and western blot assays were used to detect the expression level of AXIN1 and other key proteins. CCK-8 assays and cell apoptosis assays were used to detect cell proliferation and cell apoptosis. Results: AXIN1 was significantly overexpressed in an in vitro model of I/R injury. Knockdown of AXIN1 significantly restored the cell proliferation inhibition caused by IR injury, while inhibiting apoptosis and inflammation. Further mechanistic studies revealed that the transcription factor c-Myc could regulate the expression of AXIN1. The effects of I/R injury on AC16 cells after overexpression of c-Myc were reversed by knockdown of AXIN1. Meanwhile, AXIN1 could regulate the SIRT1/p53/Nrf 2 pathway. Conclusion: Our results show an important role for AXIN1 and provide new targets for avoiding and treating I/R injury.
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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 Socratic graph.