ArticleExperimental and therapeutic medicine2018
Relaxin ameliorates high glucose-induced cardiomyocyte hypertrophy and apoptosis via the Notch1 pathway.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 26 citations in OpenAlex.
- TUBB4A relieves high glucose-induced cardiomyocyte hypertrophy and apoptosis through the regulation of ubiquitination and activation of the NOTCH signaling pathway.Cytotechnology · 2025Article
- Protective Effects of Relaxin 2 (RLXH2) against Hypoxia-Induced Oxidative Damage and Cell Death via Activation of The Nrf2/HO-1 Signalling Pathway in Gastric Cancer Cells.Cell journal · 2023Article
- Endothelial-cell-mediated mechanism of coronary microvascular dysfunction leading to heart failure with preserved ejection fraction.Heart failure reviews · 2023Review
- Gut microbiota: A new therapeutic target for diabetic cardiomyopathy.Frontiers in pharmacology · 2022Review
- microRNA-133a exerts tumor suppressive role in oral squamous cell carcinoma through the Notch signaling pathway via downregulation of CTBP2.Cancer gene therapy · 2022Article
- Human Relaxin-2 (Serelaxin) Attenuates Oxidative Stress in Cardiac Muscle Cells Exposed In Vitro to Hypoxia-Reoxygenation. Evidence for the Involvement of Reduced Glutathione Up-Regulation.Antioxidants (Basel, Switzerland) · 2020Article
- Retracted Article: Knockdown of TUG1 aggravates hypoxia-induced myocardial cell injuryRSC advances · 2019Article
- Overexpression of small ubiquitin‑like modifier 2 ameliorates high glucose‑induced reductions in cardiomyocyte proliferation via the transforming growth factor‑β/Smad pathway.Molecular medicine reports · 2018Article
- Blockade of RBP-J-Mediated Notch Signaling Pathway Exacerbates Cardiac Remodeling after Infarction by Increasing Apoptosis in Mice.BioMed research international · 2018Article
- Activating Cannabinoid Receptor 2 Protects Against Diabetic Cardiomyopathy Through Autophagy Induction.Frontiers in pharmacology · 2018Article
- Relaxin as a Therapeutic Target for the Cardiovascular Complications of Diabetes.Frontiers in pharmacology · 2018Review
- The Melanocortin MC5R as a New Target for Treatment of High Glucose-Induced Hypertrophy of the Cardiac H9c2 Cells.Frontiers in physiology · 2018Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to investigate the role of relaxin (RLX) on high glucose (HG)-induced cardiomyocyte hypertrophy and apoptosis, as well as the possible molecular mechanism. H9c2 cells were exposed to 33 mmol/l HG with or without RLX (100 nmol/ml). Cell viability, apoptosis, oxidative stress, cell hypertrophy and the levels of Notch1, hairy and enhancer of split 1 (hes1), atrial natriuretic polypeptide (ANP), brain natriuretic peptide (BNP), manganese superoxide dismutase (MnSOD), cytochrome C and caspase-3 were assessed in cardiomyocytes. Compared with the HG group, the viability of H9c2 cells was increased by RLX in a time- and dose-dependent manner, and was accompanied with a significant reduction in apoptosis. Furthermore, RLX significantly suppressed the formation of reactive oxygen species and malondialdehyde, and enhanced the activity of SOD. In addition, the levels of ANP, BNP, cytochrome C and caspase-3 were increased and Notch1, hes1 and MnSOD were inhibited in the HG group compared with those in the normal group. However, the Notch inhibitor DAPT almost abolished the protective effects of RLX. These results suggested that RLX protected cardiomyocytes from HG-induced hypertrophy and apoptosis partly through a Notch1-dependent pathway, which may be associated with reducing oxidative stress.
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