ArticleMolecular medicine reports2019
Calcium‑sensing receptor promotes high glucose‑induced myocardial fibrosis via upregulation of the TGF‑β1/Smads pathway in cardiac fibroblasts.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Cardioprotective Role of CalhexCell biochemistry and biophysics · 2026Review
- Calcium dysregulation in diabetic cardiomyopathy & heart failure with preserved ejection fraction.Frontiers in cardiovascular medicine · 2026Review
- The role of myocardial fibrosis in the diabetic cardiomyopathy.Diabetology & metabolic syndrome · 2025Review
- Research progress on cellular behavior of CaSR in cardiovascular diseases.Frontiers in immunology · 2025Review
- The endogenous glutamatergic transmitter system promotes collagen synthesis in cardiac fibroblasts under hypoxia.Frontiers in cardiovascular medicine · 2025Article
- Exogenous Spermidine Alleviates Diabetic Myocardial Fibrosis Via Suppressing Inflammation and Pyroptosis in db/db MiceBalkan medical journal · 2023Article
- Activation of Kir2.1 improves myocardial fibrosis by inhibiting CaActa biochimica et biophysica Sinica · 2023Article
- Central role of cardiac fibroblasts in myocardial fibrosis of diabetic cardiomyopathy.Frontiers in endocrinology · 2023Review
- Calcium-Sensing Receptor (CaSR)-Mediated Intracellular Communication in Cardiovascular Diseases.Cells · 2022Review
- Upregulation of TGF-β type II receptor in high glucose-induced vascular smooth muscle cells.Molecular biology reports · 2022Article
- Ginsenoside Rg1 attenuates mechanical stress-induced cardiac injury via calcium sensing receptor-related pathway.Journal of ginseng research · 2021Article
- Fibrosis of the diabetic heart: Clinical significance, molecular mechanisms, and therapeutic opportunities.Advanced drug delivery reviews · 2021Review
- Non-ischemic dilated cardiomyopathy and cardiac fibrosis.Heart failure reviews · 2021Review
- Protective Effects of Huangqi Shengmai Yin on Type 1 Diabetes-Induced Cardiomyopathy by Improving Myocardial Lipid Metabolism.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Calcium-Sensing Receptor Participates in High Glucose-Induced EndMT in Primary Human Aortic Endothelial Cells.Frontiers in physiology · 2020Article
- Chemerin/CMKLR1 Axis Promotes Inflammation and Pyroptosis by Activating NLRP3 Inflammasome in Diabetic Cardiomyopathy Rat.Frontiers in physiology · 2020Article
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9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic cardiomyopathy (DCM) is a major complication of diabetes and myocardial fibrosis is its major pathological feature. Calcium‑sensing receptor (CaSR) is a G protein‑coupled receptor and participates in the regulation of calcium homeostasis; it is implicated in a range of diseases, including myocardial ischemia/reperfusion injury, myocardial infarction and pulmonary hypertension. However, whether CaSR is associated with myocardial fibrosis in DCM has remained elusive. In the present study, type 1 diabetic (T1D) rats and primary neonatal rat cardiac fibroblasts (CFs) were used to observe changes in CaSR to assess its potential as an indicator of myocardial fibrosis. The in vivo experiments revealed that in the T1D and CaSR agonist (R568) groups, evident collagen (Col)‑I and ‑III deposition was present after 12 weeks. Furthermore, the in vitro experiment indicated that the levels of transforming growth factor (TGF)‑β1, phosphorylated (p‑) protein kinase C, p‑p38, p‑Smad2, TβRI, TβRII, along with the intracellular Ca2+ levels and the content of TGF‑β1 in the culture medium were significantly increased in a high‑glucose (HG) group and an R568‑treated group. Treatment with the CaSR inhibitor Calhex231 significantly inhibited the abovementioned changes. Collectively, the results indicated that the increase of CaSR expression in CFs may induce intracellular Ca2+ increases and the activation of TGF‑β1/Smads, and enhance the proliferation of CFs, along with the excessive deposition of Col, resulting in myocardial fibrosis. The present results indicate an important novel mechanism for HG‑induced myocardial fibrosis and suggest that CaSR may be a promising potential therapeutic target for DCM.
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