ArticleHeliyon2025
TRIM26 exacerbates pathological cardiac hypertrophy by activating TAK1.
Article in Heliyon, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
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Who cites it
3 citing papers in PubMed.
- RASSF1A and its epigenetic dysregulation in genitourinary cancer: a current update.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Targeted Delivery of Schisandrin A to Cardiac Endothelium Alleviates Myocardial Ischemia-Reperfusion Injury via Suppression of Ferroptosis.International journal of nanomedicine · 2026Article
- Ubiquitination-mediated protein homeostasis in cardiovascular diseases: molecular mechanisms and therapeutic opportunities.American journal of cardiovascular disease · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pathological myocardial hypertrophy can induce heart failure with high mortality, it is necessary to explore its pathogenesis. Tripartite motif-containing 26 (TRIM26) belongs to the multidomain E3 ubiquitin ligase family. We observed increased expression of TRIM26 in the myocardium of C57BL/6 mice subjected to transverse aortic constriction (TAC) surgery and neonatal rat cardiomyocytes (NRCMs) treated with phenylephrine (PE). To evaluate the role of TRIM26 in pathological cardiac hypertrophy, we generated
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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.