ArticleHerz2015
Mitochondrial coupling factor 6 upregulation in hypertension-induced cardiac hypertrophy.
Article in Herz, 2015. 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
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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
1 citing paper in PubMed.
- Pathogenesis of cardiovascular diseases: effects of mitochondrial CF6 on endothelial cell function.Molecular and cellular biochemistry · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMitochondrial coupling factor 6 (CF6) is a constriction factor in cardiac hypertrophy, whose mechanisms are not fully understood. MATERIALS AND
methodsHere, we established cardiac hypertrophy models for feeding spontaneously hypertensive rats (SHRs) aged 10, 20, and 30 weeks. Hemodynamic monitoring was performed during the feeding program to ensure the success of the model.
resultsCardiac hypertrophy, but not fibrosis, occurred in the 10-, 20-, and 30-week-old SHRs. No significant changes in CF6 gene expression were detected by RT-PCR in any of the SHR groups as compared with the control groups (p > 0.05). ELISA assessment showed that the CF6 protein level in the 20- and 30-week-old SHRs with cardiac hypertrophy was significantly increased (vs. control, p < 0.05).
conclusionCF6 protein was upregulated in cardiac hypertrophy induced by hypertension; further mechanisms involved in this process should be investigated.
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Registered trials
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