Apelin Ameliorates High Glucose-Induced Downregulation of Connexin 43 via AMPK-Dependent Pathway in Neonatal Rat Cardiomyocytes.

Li X, Yu L, Gao J, Bi X, Zhang J, Xu S, Wang M, Chen M, Qiu F, Fu G

Aging and disease1 Feb 2018Cited by 22 (Europe PMC)

PMID29392082PMCIDPMC5772859DOI10.14336/ad.2017.0426PepBankPUB-29392082

Summary

Diabetes Mellitus is a common disorder, with increasing risk of cardiac arrhythmias. Studies have shown that altered connexin expression and gap junction remodeling under hyperglycemia contribute to the high prevalence of cardiac arrhythmias and even sudden death. Connexin 43 (Cx43), a major protein that assembles to form cardiac gap junctions, has been found to be downregulated under high glucose conditions, along with inhibition of gap junctional intercellular communication (GJIC). While, apelin, a beneficial adipokine, increases Cx43 protein expression in mouse and human embryonic stem cells during cardiac differentiation. However, it remains unknown whether apelin influences GJIC capacity in cardiomyocytes. Here, using Western blotting and dye transfer assays, we found that Cx43 protein expression was reduced and GJIC was impaired after treatment with high glucose, which, however, could be abrogated after apelin treatment for 48 h. We also found that apelin increased Cx43 expression under normal glucose. Real-time PCR showed that the Cx43 mRNA was not significantly affected under high glucose conditions in the presence of apelin or high glucose and apelin. High glucose decreased the phosphorylation of AMPKα; however, apelin activated AMPKα. Interestingly, we found that Cx43 expression was increased after treatment with AICAR, an activator of AMPK signaling. AMPKα inhibition mediated with transfection of siRNA-AMPKα1 and siRNA-AMPKα2 abolished the protective effect of apelin on Cx43 expression. Our data suggest that apelin attenuates high glucose-induced Cx43 downregulation and improves the loss of functional gap junctions partly through the AMPK pathway.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study1

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Studies that did not test the peptide alone1

In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking AICAR (acadesine).

01LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism
In neonatal rat cardiomyocytes, AICAR increased connexin 43 expression.
In plain wordsIn cells from newborn rat hearts, AICAR increased connexin 43 expression.
Peptide
AICAR (acadesine)
Outcome
IncreaseConnexin 43 expression
Study
ratn: not reported in source
Neonatal rat cardiomyocytes
Outcome group
Receptor activity and mechanism · Cardiovascular
Source sentences
Summary
Interestingly, we found that Cx43 expression was increased after treatment with AICAR, an activator of AMPK signaling.
1 context sentence(design, population, supporting numbers)
Title · context
Apelin Ameliorates High Glucose-Induced Downregulation of Connexin 43 via AMPK-Dependent Pathway in Neonatal Rat Cardiomyocytes.
In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking AICAR (acadesine).
Show in the study text Report a problemFND-2939208201

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Version 2Current
21 Oct 2026, 15:58 UTC
Study results updated
Version 1
21 Oct 2026, 12:50 UTC
First added · source update from Europe PMC

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