ArticleHypertension (Dallas, Tex. : 1979)2014
Interferon regulatory factor 7 functions as a novel negative regulator of pathological cardiac hypertrophy.
Article in Hypertension (Dallas, Tex. : 1979), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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50 citing papers in PubMed, 98 citations in OpenAlex.
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- Sacubitril/Valsartan attenuates progression of diabetic cardiomyopathy through immunomodulation properties: an opportunity to prevent progressive disease.Cardiovascular diabetology · 2025Article
- Deubiquitinase Ubiquitin-Specific Protease 29 Ameliorates Pathological Cardiac Hypertrophy through Inhibiting Transforming Growth Factor β-Activated Kinase 1.Journal of the American Heart Association · 2025Article
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- Fas Apoptosis Inhibitory Molecule 2 Inhibits Pathological Cardiac Hypertrophy by Regulating the MAPK Signaling Pathway.Journal of the American Heart Association · 2024Article
- Local adaptation, plasticity, and evolved resistance to hypoxic cold stress in high-altitude deer mice.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Lactate regulates pathological cardiac hypertrophy via histone lactylation modification.Journal of cellular and molecular medicine · 2024Article
- Local adaptation, plasticity, and evolved resistance to hypoxic cold stress in high-altitude deer mice.bioRxiv : the preprint server for biology · 2024Article
- Endothelial cells adopt a pro-reparative immune responsive signature during cardiac injury.Life science alliance · 2024Article
- Single-cell RNA sequencing reveals the transcriptional heterogeneity of Tbx18-positive cardiac cells during heart development.Functional & integrative genomics · 2024Article
- Cellular zinc metabolism and zinc signaling: from biological functions to diseases and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Interferons and interferon-related pathways in heart disease.Frontiers in cardiovascular medicine · 2024Review
- Aortic smooth muscle TRPV4 channels regulate vasoconstriction in high salt-induced hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2023Article
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- The interaction between ferroptosis and inflammatory signaling pathways.Cell death & disease · 2023Review
- Transcriptomic profiling of cardiac tissues from SARS-CoV-2 patients identifies DNA damage.Immunology · 2023Article
- Article
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16 authors at 6 institutions in 3 countries.
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Abstract
Cardiac hypertrophy is a complex pathological process that involves multiple factors including inflammation and apoptosis. Interferon regulatory factor 7 (IRF7) is a multifunctional regulator that participates in immune regulation, cell differentiation, apoptosis, and oncogenesis. However, the role of IRF7 in cardiac hypertrophy remains unclear. We performed aortic banding in cardiac-specific IRF7 transgenic mice, IRF7 knockout mice, and the wild-type littermates of these mice. Our results demonstrated that IRF7 was downregulated in aortic banding-induced animal hearts and cardiomyocytes that had been treated with angiotensin II or phenylephrine for 48 hours. Accordingly, heart-specific overexpression of IRF7 significantly attenuated pressure overload-induced cardiac hypertrophy, fibrosis, and dysfunction, whereas loss of IRF7 led to opposite effects. Moreover, IRF7 protected against angiotensin II-induced cardiomyocyte hypertrophy in vitro. Mechanistically, we identified that IRF7-dependent cardioprotection was mediated through IRF7 binding to inhibitor of κB kinase-β, and subsequent nuclear factor-κB inactivation. In fact, blocking nuclear factor-κB signaling with cardiac-specific inhibitors of κBα(S32A/S36A) super-repressor transgene counteracted the adverse effect of IRF7 deficiency. Conversely, activation of nuclear factor-κB signaling via a cardiac-specific conditional inhibitor of κB kinase-β(S177E/S181E) (constitutively active) transgene negated the antihypertrophic effect of IRF7 overexpression. Our data demonstrate that IRF7 acts as a novel negative regulator of pathological cardiac hypertrophy by inhibiting nuclear factor-κB signaling and may constitute a potential therapeutic target for pathological cardiac hypertrophy.
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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.