ArticleScience advances2019
The immunoproteasome catalytic β5i subunit regulates cardiac hypertrophy by targeting the autophagy protein ATG5 for degradation.
Article in Science advances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 90 citations in OpenAlex.
- The role of immunoproteasome in diabetes and diabetes-related complications.Genes & diseases · 2026Review
- UBA1 promotes cardiac hypertrophy by suppressing autophagy via targeting ATG5 for ubiquitination.Cell communication and signaling : CCS · 2026Article
- Thymoquinone Protects Against Cardiac Hypertrophy via PPAR-γ/PI3K/Akt Pathway.Journal of cellular and molecular medicine · 2026Article
- Targeting the Ubiquitin-Proteasome System in Atrial Fibrillation: Mechanistic Insights and Translational Perspectives.Current issues in molecular biology · 2025Review
- 4-Hydroxychalcone alleviated Angiotensin II-induced atrial fibrillation via immunoproteasome-IKK-NF-κB signaling pathway modulation.Journal of molecular medicine (Berlin, Germany) · 2025Article
- Current landscape of the immunoproteasome: implications for disease and therapy.Cell death discovery · 2025Review
- The mitochondrial hub gene UCHL1 May serve as a potential biomarker for diagnosing diabetic cardiomyopathy: a comprehensive integration of biological pathways.BMC medical genomics · 2025Article
- Ubiquitin Specific Protease 9X Regulates the Activation of ARK5 and Promotes Progression of Fibrotic Remodeling.JACC. Basic to translational science · 2025Article
- GLA deficiency causes cardiac hypertrophy via enhanced autophagy.Science China. Life sciences · 2025Article
- The gut microbiota metabolite trimethylamine N-oxide promotes cardiac hypertrophy by activating the autophagic degradation of SERCA2a.Communications biology · 2025Article
- Thymoquinone mitigates cardiac hypertrophy by activating adaptive autophagy via the PPAR‑γ/14‑3‑3γ pathway.International journal of molecular medicine · 2025Article
- β-Hydroxybutyrate and Citrate Synthase as Potential Diagnostic Biomarkers in Aging-Related Atrial Fibrillation.Journal of cardiovascular translational research · 2025Article
- Psmb8 inhibits mitochondrial fission and alleviates myocardial ischaemia/reperfusion injury by targeting Drp1 degradation.Cell death & disease · 2024Article
- Regulated Cell Death Pathways in Pathological Cardiac Hypertrophy.Reviews in cardiovascular medicine · 2024Review
- Targeting the immunoproteasome in hypothalamic neurons as a novel therapeutic strategy for high-fat diet-induced obesity and metabolic dysregulation.Journal of neuroinflammation · 2024Article
- Immunoproteasomal Processing of IsoLG-Adducted Proteins Is Essential for Hypertension.Circulation research · 2024Article
- Pharmacological induction of autophagy reduces inflammation in macrophages by degrading immunoproteasome subunits.PLoS biology · 2024Article
- ATGL deficiency aggravates pressure overload-triggered myocardial hypertrophic remodeling associated with the proteasome-PTEN-mTOR-autophagy pathway.Cell biology and toxicology · 2023Article
- The immunoproteasome subunit β2i ameliorates myocardial ischemia/reperfusion injury by regulating Parkin-Mfn1/2-mediated mitochondrial fusion.Cellular and molecular life sciences : CMLS · 2023Article
- Ursolic Acid Ameliorates Myocardial Ischaemia/Reperfusion Injury by Improving Mitochondrial Function via Immunoproteasome-PP2A-AMPK Signalling.Nutrients · 2023Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pathological cardiac hypertrophy eventually leads to heart failure without adequate treatment. The immunoproteasome is an inducible form of the proteasome that is intimately involved in inflammatory diseases. Here, we found that the expression and activity of immunoproteasome catalytic subunit β5i were significantly up-regulated in angiotensin II (Ang II)-treated cardiomyocytes and in the hypertrophic hearts. Knockout of β5i in cardiomyocytes and mice markedly attenuated the hypertrophic response, and this effect was aggravated by β5i overexpression in cardiomyocytes and transgenic mice. Mechanistically, β5i interacted with and promoted ATG5 degradation thereby leading to inhibition of autophagy and cardiac hypertrophy. Further, knockdown of ATG5 or inhibition of autophagy reversed the β5i knockout-mediated reduction of cardiomyocyte hypertrophy induced by Ang II or pressure overload. Together, this study identifies a novel role for β5i in the regulation of cardiac hypertrophy. The inhibition of β5i activity may provide a new therapeutic approach for hypertrophic diseases.
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