ArticleBiochemical and biophysical research communications2015
Transgenic over-expression of YY1 induces pathologic cardiac hypertrophy in a sex-specific manner.
Article in Biochemical and biophysical research communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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
8 citing papers in PubMed, 9 citations in OpenAlex.
- Sex-dependent epigenetic disruption of YY1 binding by prenatal BPA exposure downregulates Matr3 and alters Agap1 splicing in the offspring hippocampus.Biology of sex differences · 2025Article
- Pim3 up-regulation by YY1 contributes to diabetes-induced cardiac hypertrophy and heart failure.Iranian journal of basic medical sciences · 2025Article
- Article
- The biological implications of Yin Yang 1 in the hallmarks of cancer.Theranostics · 2020Review
- Upregulation of Yy1 Suppresses Dilated Cardiomyopathy caused by Ttn insufficiency.Scientific reports · 2019Article
- MicroRNA Let-7d-3p Contributes to Cardiac Protection via Targeting HMGA2.International journal of molecular sciences · 2019Article
- Pharmacological induction of hypoxia-inducible transcription factor ARNT attenuates chronic kidney failure.The Journal of clinical investigation · 2018Article
- A Systems Biology Approach to Investigating Sex Differences in Cardiac Hypertrophy.Journal of the American Heart Association · 2017Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
YY1 can activate or repress transcription of various genes. In cardiac myocytes in culture YY1 has been shown to regulate expression of several genes involved in myocyte pathology. YY1 can also acutely protect the heart against detrimental changes in gene expression. In this study we show that cardiac over-expression of YY1 induces pathologic cardiac hypertrophy in male mice, measured by changes in gene expression and lower ejection fraction/fractional shortening. In contrast, female animals are protected against pathologic gene expression changes and cardiac dysfunction. Furthermore, we show that YY1 regulates, in a sex-specific manner, the expression of mammalian enable (Mena), a factor that regulates cytoskeletal actin dynamics and whose expression is increased in several models of cardiac pathology, and that Mena expression in humans with heart failure is sex-dependent. Finally, we show that sex differences in YY1 expression are also observed in human heart failure. In summary, this is the first work to show that YY1 has a sex-specific effect in the regulation of cardiac pathology.
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