Evidence mapPaperPMID 36497087Full record

ArticleCells2022

Liraglutide Improves the Angiogenic Capability of EPC and Promotes Ischemic Angiogenesis in Mice under Diabetic Conditions through an Nrf2-Dependent Mechanism.

Xiaoqing Yan, Yue Su, Xia Fan, Hui Chen, Zixian Lu, Zijuan Liu, Yingjian Li, Mei Yi, Guigui Zhang, Chunjie Gu and 7 more

Abstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Liraglutide Promotes Diabetic Wound Healing via Myo1c/Dock5.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  9. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors.

Xiaoqing YanChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, China.
Yue SuThe Second School of Medicine, Wenzhou Medical University, Wenzhou 325027, China.
Xia FanChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, China.
Hui ChenChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, China.
Zixian LuChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, China.
Zijuan LiuChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, China.
Yingjian LiChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, China.
Mei YiChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, China.
Guigui ZhangChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, China.
Chunjie GuChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, China.
Kai WangDepartment of Pediatrics, Endocrinology and Metabolism, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325200, China.ORCID 0000-0002-3615-0663
Jiamin WuChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, China.
Da SunInstitute of Life Sciences, Wenzhou University, Wenzhou 325200, China.ORCID 0000-0001-7747-9951
Yikai ZhangDepartment of Endocrinology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310058, China.
Chi ZhangThe Third Affiliated Hospital of Wenzhou Medical University, Wenzhou 325200, China.
Xiaozhen DaiSchool of Biosciences and Technology, Chengdu Medical College, Chengdu 610500, China.
Chao ZhengThe Second School of Medicine, Wenzhou Medical University, Wenzhou 325027, China.ORCID 0000-0002-2779-0255

Funding

Basic Scientific Research Foundation of Wenzhou Medical University KYYW201907Disciplinary Construction Innovation Team Foundation of Chengdu Medical College CMC-XK-2101National Key R&D Program of China 2017YFA0506000National Natural Science Foundation of China 51901160National Natural Science Foundation of China 81873466National Natural Science Foundation of China 82070833National Natural Science Foundation of China 82073843National Natural Science Foundation of China 82170420Natural Science Foundation of Zhejiang Province LY22H020005Natural Science Foundation of Zhejiang Province LY22H070005Natural Science Foundation of Zhejiang Province LZ19H020001Zhejiang provincial key research & development program 2021C03070
6 · The paper itself

Abstract

The impairment in endothelial progenitor cell (EPC) functions results in dysregulation of vascular homeostasis and dysfunction of the endothelium under diabetic conditions. Improving EPC function has been considered as a promising strategy for ameliorating diabetic vascular complications. Liraglutide has been widely used as a therapeutic agent for diabetes. However, the effects and mechanisms of liraglutide on EPC dysfunction remain unclear. The capability of liraglutide in promoting blood perfusion and angiogenesis under diabetic conditions was evaluated in the hind limb ischemia model of diabetic mice. The effect of liraglutide on the angiogenic function of EPC was evaluated by cell scratch recovery assay, tube formation assay, and nitric oxide production. RNA sequencing was performed to assess the underlying mechanisms. Liraglutide enhanced blood perfusion and angiogenesis in the ischemic hindlimb of db/db mice and streptozotocin-induced type 1 diabetic mice. Additionally, liraglutide improved tube formation, cell migration, and nitric oxide production of high glucose (HG)-treated EPC. Assessment of liraglutide target pathways revealed a network of genes involved in antioxidant activity. Further mechanism study showed that liraglutide decreased the production of reactive oxygen species and increased the activity of nuclear factor erythroid 2-related factor 2 (Nrf2). Nrf2 deficiency attenuated the beneficial effects of liraglutide on improving EPC function and promoting ischemic angiogenesis under diabetic conditions. Moreover, liraglutide activates Nrf2 through an AKT/GSK3β/Fyn pathway, and inhibiting this pathway abolished liraglutide-induced Nrf2 activation and EPC function improvement. Overall, these results suggest that Liraglutide represents therapeutic potential in promoting EPC function and ameliorating ischemic angiogenesis under diabetic conditions, and these beneficial effects relied on Nrf2 activation.

Indexed as

Diabetes Mellitus, ExperimentalEndothelial Progenitor CellsLiraglutideNF-E2-Related Factor 2AnimalsIschemiaMiceNitric OxideLiraglutideNF-E2-Related Factor 2Nitric Oxideangiogenesisdiabetesendothelial progenitor cellsliraglutideNrf2

Identifiers

PMID36497087
PMCPMC9736458

What Socratic holds

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Registered trials

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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 Socratic graph.