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Study · PubMed tag: none · 2019

Retracted

GLP-1 receptor agonist lixisenatide protects against high free fatty acids-induced oxidative stress and inflammatory response.

Zhao Q, Xu H, Zhang L, Liu L, Wang L

Artificial cells, nanomedicine, and biotechnology1 Dec 2019Cited by 10 (Europe PMC)

PMID31174433 (opens in a new tab)DOI10.1080/21691401.2019.1620248 (opens in a new tab)PepBankPUB-31174433
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Summary

Increased free fatty acids (FFA) are one of the risk factors for type 2 diabetes. FFA also contribute to endothelial dysfunction in both the prediabetes and diabetes conditions. Therefore, FFA are an important link between diabetes and endothelial dysfunction. In therapeutic application, GLP-1 receptor agonists have been implemented to lower blood glucose in diabetes. Here, we investigate the role of the common clinically used GLP-1 receptor agonist lixisenatide in endothelial cells. We demonstrate that lixisenatide could protect endothelial cells from high FFA-induced toxicity and cell death. Lixisenatide also suppresses FFA-caused cellular ROS generation and production of the lipid oxidation byproduct 4-HNE. Lixisenatide inhibits FFA-triggered production of TNF-α, IL-6, VCAM-1 and ICAM-1. The presence of lixisenatide in co-culture experiments suppresses adhesion of monocytes to endothelial cells. Moreover, lixisenatide ameliorates FFA-induced decreased eNOS phosphorylation and NO reduction. We also demonstrate that lixisenatide inhibits FFA-induced IκBα activation, nuclear p65 translocation and NF-κB activation. This evidence indicates that lixisenatide suppresses activation of the NF-κB pathway in endothelial cells. Collectively, our findings suggest that lixisenatide might have therapeutic potential to modulate diabetes-associated vascular complications.
CC BYText from Europe PMC. No result points at this text yet.

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Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    27 Oct 2026, 16:37 UTC

    Status changed: status, notices · status retracted · status notice from Retraction Watch (Crossref)

  2. Version 1

    27 Oct 2026, 16:36 UTC

    First added · status retracted · source update from Europe PMC

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