Evidence mapPaperPMID 36738369Full record

ArticleCardiovascular drugs and therapy2024

Sitagliptin Ameliorates Creb5/lncRNA ENSMUST00000213271-Mediated Vascular Endothelial Dysfunction in Obese Mice.

Yi Zong, Xiaorui Wang, Yi Zhang, Na Tan, Yan Zhang, Li Li, Limei Liu

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Article in Cardiovascular drugs and therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
1.0field-weighted citation impact, top 22% of its field
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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. Review
4 · The record

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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

7 authors at 2 institutions in 1 country.

Yi Zong *Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, China.
Xiaorui Wang *Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, China.
Yi ZhangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, China.
Na TanDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, China.
Yan ZhangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, China.
Li LiDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, China.
Limei LiuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, China. liulm@bjmu.edu.cn.
Peking University · CNMinistry of Education of the People's Republic of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeObesity is mediated by the changes in dyslipidemia, oxidative stress, and inflammation, leading to vascular endothelial dysfunction. Glucagon-like peptide-1 (GLP-1) analogues and dipeptidyl peptidase-4 inhibitors prevent the development of endothelial dysfunction. However, the underlying mechanism still remains largely unclear. Long non-coding RNAs (lncRNAs), one class of non-coding small RNAs, have been shown to exert a regulatory impact on the endothelial function in obesity. This study aimed to investigate whether the elevation of GLP-1 by a DPP-4 inhibitor sitagliptin improved vascular endothelial function by modulating lncRNAs in obese mice and to clarify the underlying molecular mechanism.

methodsMale C57BL/6J mice were fed a high-fat diet for 4 months to induce obesity and some obese mice were treated with sitagliptin for the last 1 month. Levels of total cholesterol (TC), high-density lipoprotein (HDL), low-density lipoprotein (LDL), and glucagon-like peptide-1 (GLP-1) in plasma were detected by ELISA. LncRNA expression profile was analyzed via microarray. Aortic relaxations were examined by myograph. Protein expressions and phosphorylations were determined using western blot. The differentially expressed lncRNAs were validated using qRT-PCR.

resultsObese mice exhibited increased levels of TC and LDL, decreased concentrations of HDL and GLP-1 in plasma, and impaired aortic endothelium-dependent relaxations; such effects could be reversed by sitagliptin. Moreover, the altered expression profile of lncRNAs in the obese mouse aortae could be modulated by sitagliptin. Consistent with microarray analysis, qRT-PCR also revealed that lncRNA ENSMUST00000213271 was up-regulated in obese mouse aortae and aortic endothelial cells (ECs), which could be down-regulated by sitagliptin. Creb5 silencing reduced lncRNA ENSMUST00000213271 in obese mouse ECs. Knockdown of either Creb5 or lncRNA ENSMUST00000213271 restored the activation of AMPK/eNOS in obese mouse ECs. Furthermore, sitagliptin also suppressed Creb5 and lncRNA ENSMUST00000213271 and increased the phosphorylations of AMPK and eNOS in obese mice.

conclusionCreb5/lncRNA ENSMUST00000213271 mediated vascular endothelial dysfunction through inhibiting AMPK/eNOS cascade in obesity. Elevation of GLP-1 by sitagliptin possibly improved endothelial function by suppressing Creb5/lncRNA ENSMUST00000213271 and subsequently restoring AMPK/eNOS activation in obese mice. This study will provide new evidence for the benefits of GLP-1 against vasculopathy in obesity.

Indexed as

Diet, High-FatDipeptidyl-Peptidase IV InhibitorsEndothelium, VascularGlucagon-Like Peptide 1Mice, Inbred C57BLObesityRNA, Long NoncodingSitagliptin PhosphateAnimalsCyclic AMP Response Element-Binding ProteinDisease Models, AnimalEndothelial CellsMaleMiceMice, ObesePhosphorylationCyclic AMP Response Element-Binding ProteinDipeptidyl-Peptidase IV InhibitorsGlucagon-Like Peptide 1RNA, Long NoncodingSitagliptin PhosphateCyclic AMP-responsive element-binding protein 5Endothelial functionGlucagon-like peptide-1Long noncoding RNAObesity

Identifiers

PMID36738369
OpenAlexW4319216033

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.