ArticleJournal of cellular and molecular medicine2020
Zinc finger protein 91 loss induces cardiac hypertrophy through adenosine A1 receptor down-regulation under pressure overload status.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Cooperative regulation of Zhx1 and hnRNPA1 drives the cardiac progenitor-specific transcriptional activation during cardiomyocyte differentiation.Cell death discovery · 2023Article
- Full-Length Transcriptome Sequencing: An Insight Into the Dog Model of Heart Failure.Frontiers in cardiovascular medicine · 2021Article
- Zinc finger protein 91 loss induces cardiac hypertrophy through adenosine A1 receptor down-regulation under pressure overload status.Journal of cellular and molecular medicine · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The function of zfp91 is mainly studied in vitro, but there is no study in vivo. Accumulative data suggest that zfp91 may be an important gene to regulate all aspects of human response. However, there are no data to date about the function of zfp91 on cardiac homeostasis. Thus, we aimed to observe the role of zfp91 gene in mouse cardiomyocytes on myocardial homeostasis and related mechanisms under pressure overload. In the study, zfp91 mRNA and protein levels were significantly reduced in TAC-operated WT mice as compared with controls. Genetic ablation of zfp91 dramatically led to pathological cardiac dysfunction and hypertrophy after transverse aortic constriction (TAC). Adenosine A1 receptor (Adora1) mRNA and protein expressions were significantly down-regulated in the heart of zfp91-deletion mice with TAC. Zfp91 overexpression reversed isoproterenol-induced cardiomyocyte hypertrophy, which was abolished by selective Adora1 antagonist. Dual-luciferase reporter and ChIP-qPCR assays indicated that zfp91 acted on Adora1 promoter through its binding site. Last, Adora1 agonist rescued heart dysfunction and cardiac hypertrophy in zfp91 loss mice after TAC. Zfp91 may transcriptionally regulate Adora1 expression in the heart, which mainly maintained cardiac homeostasis under pressure overload status. It will provide a new approach to treat cardiac hypertrophy.
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