Evidence map›Paper›PMID 35508613›Full record

ArticleCell death discovery2022

LncRNA LYPLAL1-DT screening from type 2 diabetes with macrovascular complication contributes protective effects on human umbilical vein endothelial cells via regulating the miR-204-5p/SIRT1 axis.

Xiao Zhu, Yihan Liu, Jia Cui, Jianyi Lv, Changlong Li, Jing Lu, Xueyun Huo, Jingtao Dou, Zhigang Bai, Zhenwen Chen and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 21 citations in OpenAlex.

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  12. MicroRNAs in diabetic macroangiopathy.Cardiovascular diabetology · 2024
    Review
  13. Salvianolic acid A alleviates HScientific reports · 2024
    Article
  14. Article
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  16. Review
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  18. Review
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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

11 authors at 2 institutions in 1 country.

Xiao ZhuDepartment of medical genetics and biological development, School of Basic Medical Sciences, Capital Medical University, No.10 Xitoutiao, Youanmen, Fengtai District, Beijing, 100069, China.
Yihan LiuDepartment of medical genetics and biological development, School of Basic Medical Sciences, Capital Medical University, No.10 Xitoutiao, Youanmen, Fengtai District, Beijing, 100069, China.
Jia CuiDepartment of Endocrinology, Chinese PLA General Hospital, Beijing, 100853, China.
Jianyi LvDepartment of medical genetics and biological development, School of Basic Medical Sciences, Capital Medical University, No.10 Xitoutiao, Youanmen, Fengtai District, Beijing, 100069, China.
Changlong LiDepartment of medical genetics and biological development, School of Basic Medical Sciences, Capital Medical University, No.10 Xitoutiao, Youanmen, Fengtai District, Beijing, 100069, China.
Jing LuDepartment of medical genetics and biological development, School of Basic Medical Sciences, Capital Medical University, No.10 Xitoutiao, Youanmen, Fengtai District, Beijing, 100069, China.
Xueyun HuoDepartment of medical genetics and biological development, School of Basic Medical Sciences, Capital Medical University, No.10 Xitoutiao, Youanmen, Fengtai District, Beijing, 100069, China.
Jingtao DouDepartment of Endocrinology, Chinese PLA General Hospital, Beijing, 100853, China.
Zhigang BaiDepartment of General Surgery, Beijing Friendship Hospital, Capital Medical University, Beijing Key Laboratory of Cancer Invasion and Metastasis Research & National Clinical Research Center for Digestive Diseases, Beijing, China.
Zhenwen ChenDepartment of medical genetics and biological development, School of Basic Medical Sciences, Capital Medical University, No.10 Xitoutiao, Youanmen, Fengtai District, Beijing, 100069, China.
Xiaoyan DuDepartment of medical genetics and biological development, School of Basic Medical Sciences, Capital Medical University, No.10 Xitoutiao, Youanmen, Fengtai District, Beijing, 100069, China. duduyan@ccmu.edu.cn.ORCID http://orcid.org/0000-0002-4030-7299
Capital Medical University · CNChinese PLA General Hospital · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 31772545National Natural Science Foundation of China (National Science Foundation of China) 31970512
6 · The paper itself

Abstract

Long noncoding RNAs (lncRNAs) are involved in diabetes related diseases. However, the role of lncRNAs in the pathogenesis of type 2 diabetes with macrovascular complication (DMC) has seldomly been recognized. This study screened lncRNA profiles of leukocytes from DMC patients and explored protective role of lncRNA LYPLAL1-DT in endothelial cells (EC) under high glucose (HG) and inflammatory conditions (IS). Between DMC and healthy controls, 477 differential expression lncRNAs (DE-lncRNAs) were identified. The enrichment and pathway analysis showed that most of the DE-lncRNAs belonged to inflammatory, metabolic, and vascular diseases. A total of 12 lncRNAs was validated as significant DE-lncRNAs in expanding cohorts. Furthermore, these DE-lncRNAs were shown to be significantly related to hypoxia, HG, and IS in EC, especially lncRNA LYPLAL1-DT. LYPLAL1-DT overexpression results in the promotion of the proliferation, and migration of EC, as well as an elevation of autophagy. Overexpressed LYPLAL1-DT reduces the adhesion of monocytes to EC, boosts anti-inflammation, and suppresses inflammatory molecules secreted in the medium. Mechanistically, LYPLAL1-DT acts as competing endogenous RNA (ceRNA) by downregulating miR-204-5p, therefore enhancing SIRT1 and protecting EC autophagy function; thus, alleviating apoptosis. Finally, exosome sequencing revealed LYPLAL1-DT expression was 4 times lower in DMC cells than in healthy samples. In general, we identified LYPLAL1-DT having protective effects on EC as ceRNA mediated through the miR-204-5p/SIRT1 pathway. Therefore, it inhibits the autophagy of EC as well as modulating systemic inflammation. This approach could be regarded as a new potential therapeutic target in DMC.

Identifiers

PMID35508613
PMCPMC9068612
OpenAlexW4229012409

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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 OpenQuestion graph.