ArticleEndocrine2017
Low-after-high glucose down-regulated Cx43 in H9c2 cells by autophagy activation via cross-regulation by the PI3K/Akt/mTOR and MEK/ERK
Article in Endocrine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- Glycemia reprograms substrate transport and shapes divergent stress responses in differentiating H9c2 cells.Cell stress · 2026Article
- DHRS13 suppresses differentiation and mitophagy in glioma via retinoic acid and mitochondrial reactive oxygen species.Nature communications · 2025Article
- The Shenlian Fumai Granule attenuates Ach-CaClFrontiers in cardiovascular medicine · 2025Article
- Apelin-13 Increases Functional Connexin-43 through Autophagy Inhibition via AKT/mTOR Pathway in the Non-Myocytic Cell Population of the Heart.International journal of molecular sciences · 2022Article
- Hypoglycemia-Exacerbated Mitochondrial Connexin 43 Accumulation Aggravates Cardiac Dysfunction in Diabetic Cardiomyopathy.Frontiers in cardiovascular medicine · 2022Article
- Article
- Dapagliflozin Improves Diabetic Cardiomyopathy by Modulating the Akt/mTOR Signaling Pathway.BioMed research international · 2022Article
- Effect of WenXin KeLi on Improvement of Arrhythmia after Myocardial Infarction by Intervening PI3K-AKT-mTOR Autophagy Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Protective Effects of Zinc on Spinal Cord Injury.Journal of molecular neuroscience : MN · 2021Review
- Adiponectin Attenuates Lipopolysaccharide-induced Apoptosis by Regulating the Cx43/PI3K/AKT Pathway.Frontiers in pharmacology · 2021Article
- Human enteroviral infection impairs autophagy in clonal INS(832/13) cells and human pancreatic islet cells.Diabetologia · 2020Article
- Salvia miltiorrhiza-Derived Sal-miR-58 Induces Autophagy and Attenuates Inflammation in Vascular Smooth Muscle Cells.Molecular therapy. Nucleic acids · 2020Article
- Escins Isolated fromFrontiers in pharmacology · 2020Article
- The long noncoding RNA THRIL knockdown protects hypoxia-induced injuries of H9C2 cells through regulating miR-99a.Cardiology journal · 2019Article
- The Role of Connexin-43 in the Inflammatory Process: A New Potential Therapy to Influence Keratitis.Journal of ophthalmology · 2019Review
- Activation of adenosine A2b receptor attenuates high glucose-induced apoptosis in H9C2 cells via PI3K/Akt signaling.In vitro cellular & developmental biology. Animal · 2018Article
- Oleic acid induces apoptosis and autophagy in the treatment of Tongue Squamous cell carcinomas.Scientific reports · 2017Article
- Calcium sensing receptor protects high glucose-induced energy metabolism disorder via blocking gp78-ubiquitin proteasome pathway.Cell death & disease · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeHypoglycemia in diabetes is a strong predictor of cardiovascular events. High-glucose have been reported to alter connexin43 expression and to promote autophagy in cardiomyocytes. We investigated whether low-after-high glucose would influence connexin43 expression and autophagy in H9c2 cells.
methodsH9c2 cells were incubated in 33.3 mM glucose for 24 h followed by 2.5 mM glucose for 2, 4, 6, or 12 h with or without chloroquine (autophagy inhibitor), U0126 (MEK
resultsCytotoxicity and early apoptosis were increased and cell proliferation was decreased after exposure to low-after-high glucose, and these results were reversed by chloroquine and U0126 but were aggravated by LY294002. Connexin43 expression was downregulated in a time-dependent manner and was accompanied by upregulated expression of LC3-II, Beclin-1, p62, p-Akt, p-mTOR, and p-ERK
conclusionCulturing H9c2 cells under low-after-high glucose downregulated connexin43 by promoting autophagy through a mechanism involving the PI3K/Akt/mTOR and MEK/ERK
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.