ArticleNature communications2016
Suppressor of IKKɛ is an essential negative regulator of pathological cardiac hypertrophy.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 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
38 citing papers in PubMed, 69 citations in OpenAlex.
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- Ubiquitin specific protease 38 aggravates pathological cardiac remodeling by stabilizing phospho-TBK1.International journal of biological sciences · 2024Article
- Chinese herbal formula in the treatment of metabolic dysfunction-associated steatotic liver disease: current evidence and practice.Frontiers in medicine · 2024Review
- The Relationship Between Insulin Resistance Indicated by Triglyceride and Glucose Index and Left Ventricular Hypertrophy and Decreased Left Ventricular Diastolic Function with Preserved Ejection Fraction.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- TRAF Family Member 4 Promotes Cardiac Hypertrophy Through the Activation of the AKT Pathway.Journal of the American Heart Association · 2023Article
- SWAP70 Overexpression Protects Against Pathological Cardiac Hypertrophy in a TAK1-Dependent Manner.Journal of the American Heart Association · 2023Article
- Nitidine chloride induces cardiac hypertrophy in mice by targeting autophagy-related 4B cysteine peptidase.Acta pharmacologica Sinica · 2023Article
- A high-throughput drug screening identifies luteolin as a therapeutic candidate for pathological cardiac hypertrophy and heart failure.Frontiers in cardiovascular medicine · 2023Article
- Energy substrate metabolism and oxidative stress in metabolic cardiomyopathy.Journal of molecular medicine (Berlin, Germany) · 2022Review
- Regulation of Key Immune-Related Genes in the Heart Following Burn Injury.Journal of personalized medicine · 2022Article
- Transcriptome and morphological analysis on the heart in gestational protein-restricted aging male rat offspring.Frontiers in cell and developmental biology · 2022Article
- 6-Gingerol protects against cardiac remodeling by inhibiting the p38 mitogen-activated protein kinase pathway.Acta pharmacologica Sinica · 2021Article
- Regulation of pyroptosis in cardiovascular pathologies: Role of noncoding RNAs.Molecular therapy. Nucleic acids · 2021Review
- TANK Promotes Pressure Overload Induced Cardiac HypertrophyFrontiers in cardiovascular medicine · 2021Article
- Short-Term Inhalation of Ultrafine Zinc Particles Could Alleviate Cardiac Dysfunctions in Rats of Myocardial Infarction.Frontiers in bioengineering and biotechnology · 2021Article
- Melatonin alleviates angiotensin-II-induced cardiac hypertrophy via activating MICU1 pathway.Aging · 2020Article
- Deubiquitinase Ubiquitin-Specific Protease 10 Deficiency Regulates Sirt6 signaling and Exacerbates Cardiac Hypertrophy.Journal of the American Heart Association · 2020Article
- Nrf2 mitigates prolonged PM2.5 exposure-triggered liver inflammation by positively regulating SIKE activity: Protection by Juglanin.Redox biology · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
17 authors at 6 institutions in 2 countries.
Funding
Abstract
Although pathological cardiac hypertrophy represents a leading cause of morbidity and mortality worldwide, our understanding of the molecular mechanisms underlying this disease is still poor. Here, we demonstrate that suppressor of IKKɛ (SIKE), a negative regulator of the interferon pathway, attenuates pathological cardiac hypertrophy in rodents and non-human primates in a TANK-binding kinase 1 (TBK1)/AKT-dependent manner. Sike-deficient mice develop cardiac hypertrophy and heart failure, whereas Sike-overexpressing transgenic (Sike-TG) mice are protected from hypertrophic stimuli. Mechanistically, SIKE directly interacts with TBK1 to inhibit the TBK1-AKT signalling pathway, thereby achieving its anti-hypertrophic action. The suppression of cardiac remodelling by SIKE is further validated in rats and monkeys. Collectively, these findings identify SIKE as a negative regulator of cardiac remodelling in multiple animal species due to its inhibitory regulation of the TBK1/AKT axis, suggesting that SIKE may represent a therapeutic target for the treatment of cardiac hypertrophy and heart failure.
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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.