ArticleCell death & disease2017
Calcium sensing receptor protects high glucose-induced energy metabolism disorder via blocking gp78-ubiquitin proteasome pathway.
Article in Cell death & disease, 2017. 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 20 papers.
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Who cites it
20 citing papers in PubMed, 38 citations in OpenAlex.
- Mitochondrial quality control in diabetes mellitus and complications: molecular mechanisms and therapeutic strategies.Cell death & disease · 2025Review
- Mitochondrial Dysfunction in HFpEF: Potential Interventions Through Exercise.Journal of cardiovascular translational research · 2025Review
- Calcium Ion Attenuates Transforming Growth Factor β1-Induced Extracellular Matrix Accumulation by Inducing Smad2 Degradation through the Proteasome Pathway.Bulletin of experimental biology and medicine · 2024Article
- Calcium-Sensing Receptor (CaSR)-Mediated Intracellular Communication in Cardiovascular Diseases.Cells · 2022Review
- Mitochondrial quality control in diabetic cardiomyopathy: from molecular mechanisms to therapeutic strategies.International journal of biological sciences · 2022Review
- Transcriptomics Coupled to Proteomics Reveals Novel Targets for the Protective Role of Spermine in Diabetic Cardiomyopathy.Oxidative medicine and cellular longevity · 2022Article
- Calcium-Sensing Receptor (CaSR), Its Impact on Inflammation and the Consequences on Cardiovascular Health.International journal of molecular sciences · 2021Review
- Spermine Protects Cardiomyocytes from High Glucose-Induced Energy Disturbance by Targeting the CaSR-gp78-Ubiquitin Proteasome System.Cardiovascular drugs and therapy · 2021Article
- The Diabetic Cardiomyopathy: The Contributing Pathophysiological Mechanisms.Frontiers in medicine · 2021Review
- SFRP2 Improves Mitochondrial Dynamics and Mitochondrial Biogenesis, Oxidative Stress, and Apoptosis in Diabetic Cardiomyopathy.Oxidative medicine and cellular longevity · 2021Article
- Activation of calcium‑sensing receptor‑mediated autophagy in high glucose‑induced cardiac fibrosis in vitro.Molecular medicine reports · 2020Article
- Exogenous spermine attenuates rat diabetic cardiomyopathy via suppressing ROS-p53 mediated downregulation of calcium-sensitive receptor.Redox biology · 2020Article
- Long-Lasting Exendin-4 Fusion Protein Improves Memory Deficits in High-Fat Diet/Streptozotocin-Induced Diabetic Mice.Pharmaceutics · 2020Article
- Promotion of mitochondrial fusion protects against developmental PBDE-47 neurotoxicity by restoring mitochondrial homeostasis and suppressing excessive apoptosis.Theranostics · 2020Article
- Cellular Protein Quality Control in Diabetic Cardiomyopathy: From Bench to Bedside.Frontiers in cardiovascular medicine · 2020Review
- Astragaloside IV alleviates myocardial damage induced by type 2 diabetes via improving energy metabolism.Molecular medicine reports · 2019Article
- Calcium‑sensing receptor promotes high glucose‑induced myocardial fibrosis via upregulation of the TGF‑β1/Smads pathway in cardiac fibroblasts.Molecular medicine reports · 2019Article
- Proteasome biology and therapeutics in cardiac diseases.Translational research : the journal of laboratory and clinical medicine · 2019Review
- Hepatic steatosis associated with decreased β-oxidation and mitochondrial function contributes to cell damage in obese mice after thermal injury.Cell death & disease · 2018Article
- SERUM VITAMIN D LEVELS IN DIFFERENT MORPHOLOGIC FORMS OF AGE RELATED CATARACT.Acta endocrinologica (Bucharest, Romania : 2005)Article
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic cardiomyopathy (DCM) is a major complication and fatal cause of the patients with diabetes. The calcium sensing receptor (CaSR) is a G protein-coupled receptor, which is involved in maintaining calcium homeostasis, regulating cell proliferation and apoptosis, and so on. In our previous study, we found that CaSR expression, intracellular calcium levels and cardiac function were all significantly decreased in DCM rats; however, the exact mechanism are not clear yet. The present study revealed the protective role of CaSR in myocardial energy metabolism disorder induced by high glucose (HG) as well as the underlying mechanism. Here, we demonstrated that HG decreased the expression of CaSR, mitochondrial fusion proteins (Mfn1, Mfn2), cell gap junction related proteins (Cx43, β-catenin, N-cadherin), and intracellular ATP concentration. In contrast, HG increased extracellular ATP concentration, the expression of gp78, mitochondrial fission proteins (Fis1, Drp1), and the ubiquitination levels of Mfn1, Mfn2 and Cx43. Moreover, CaSR agonist and gp78-siRNA significantly reduced the above changes. Taken together, these results suggest that HG induces myocardial energy metabolism disorder via decrease of CaSR expression, and activation of gp78-ubiquitin proteasome system. In turn, these effects disrupt the structure and function of the mitochondria and the cell gap junction, result in the reduced ATP synthesis and the increased ATP leakage. Stimulation of CaSR significantly attenuates HG-induced abnormal myocardial energy metabolism, suggesting CaSR would be a promising potential therapeutic target for DCM.
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