ArticleCell death and differentiation2020
The proteasome activator REGγ accelerates cardiac hypertrophy by declining PP2Acα-SOD2 pathway.
Article in Cell death and differentiation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07735130 (Angiotensin Receptor Blockade In Patients After Transcatheter Aortic Valve Replacement for Severe Aortic Stenosis With Left Ventricular Hypertrophy), which is not on this map. Cited by 14 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Angiotensin Receptor Blockade In Patients After Transcatheter Aortic Valve Replacement for Severe Aortic Stenosis With Left Ventricular Hypertrophy (ARBITAR) Trial
Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
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- Systems genetics analysis of human body fat distribution genes identifies adipocyte processes.Life science alliance · 2024Article
- PSME3 promotes lung adenocarcinoma development by regulating the TGF-β/SMAD signaling pathway.Translational lung cancer research · 2024Article
- Large animal models of pressure overload-induced cardiac left ventricular hypertrophy to study remodelling of the human heart with aortic stenosis.Cardiovascular research · 2024Review
- Structure, Function, and Allosteric Regulation of the 20S Proteasome by the 11S/PA28 Family of Proteasome Activators.Biomolecules · 2023Review
- NADPH Oxidase Subunit CYBB Confers Chemotherapy and Ferroptosis Resistance in Mesenchymal Glioblastoma via Nrf2/SOD2 Modulation.International journal of molecular sciences · 2023Article
- Reciprocal REGOxidative medicine and cellular longevity · 2023Article
- Anti-Diabetic Therapy, Heart Failure and Oxidative Stress: An Update.Journal of clinical medicine · 2022Review
- High fructose induces dysfunctional vasodilatation via PP2A-mediated eNOS Ser1177 dephosphorylation.Nutrition & metabolism · 2022Article
- Exercise-induced sudden cardiac death is caused by mitochondrio-nuclear translocation of AIF.Cell death & disease · 2021Article
- The double face of miR-320: cardiomyocytes-derived miR-320 deteriorated while fibroblasts-derived miR-320 protected against heart failure induced by transverse aortic constriction.Signal transduction and targeted therapy · 2021Article
- PA28γ: New Insights on an Ancient Proteasome Activator.Biomolecules · 2021Review
- DL-3-n-Butylphthalide Attenuates Myocardial Hypertrophy by Targeting Gasdermin D and Inhibiting Gasdermin D Mediated Inflammation.Frontiers in pharmacology · 2021Article
- Differentially expressed genes, lncRNAs, and competing endogenous RNAs in Kawasaki disease.PeerJ · 2021Article
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pathological cardiac hypertrophy eventually leads to heart failure without adequate treatment. REGγ is emerging as 11S proteasome activator of 20S proteasome to promote the degradation of cellular proteins in a ubiquitin- and ATP-independent manner. Here, we found that REGγ was significantly upregulated in the transverse aortic constriction (TAC)-induced hypertrophic hearts and angiotensin II (Ang II)-treated cardiomyocytes. REGγ deficiency ameliorated pressure overload-induced cardiac hypertrophy were associated with inhibition of cardiac reactive oxygen species (ROS) accumulation and suppression of protein phosphatase 2A catalytic subunit α (PP2Acα) decay. Mechanistically, REGγ interacted with and targeted PP2Acα for degradation directly, thereby leading to increase of phosphorylation levels and nuclear export of Forkhead box protein O (FoxO) 3a and subsequent of SOD2 decline, ROS accumulation, and cardiac hypertrophy. Introducing exogenous PP2Acα or SOD2 to human cardiomyocytes significantly rescued the REGγ-mediated ROS accumulation of Ang II stimulation in vitro. Furthermore, treatment with superoxide dismutase mimetic, MnTBAP prevented cardiac ROS production and hypertrophy features that REGγ caused in vivo, thereby establishing a REGγ-PP2Acα-FoxO3a-SOD2 pathway in cardiac oxidative stress and hypertrophy, indicates modulating the REGγ-proteasome activity may be a potential therapeutic approach in cardiac hypertrophy-associated disorders.
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