Evidence map›Paper›PMID 36117707›Full record

ReviewFrontiers in physiology2022

The mechanisms of glycolipid metabolism disorder on vascular injury in type 2 diabetes.

Xiatian Chen, Chengzhen Shi, Yin Wang, Hua Yu, Yu Zhang, Jiaxuan Zhang, Peifeng Li, Jinning Gao

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 2 pooled it
6.2field-weighted citation impact, top 3% 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

25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 47 citations in OpenAlex.

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  17. Antioxidant Potential ofAdvances in pharmacological and pharmaceutical sciences · 2025
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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

8 authors at 2 institutions in 1 country.

Xiatian ChenCenter for Molecular Genetics, Institute of Translational Medicine, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao, China.
Chengzhen ShiJuxian People's Hospital, Rizhao, China.
Yin WangCenter for Molecular Genetics, Institute of Translational Medicine, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao, China.
Hua YuThe Affiliated Cardiovascular Hospital of Qingdao University, Qingdao, China.
Yu ZhangCenter for Molecular Genetics, Institute of Translational Medicine, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao, China.
Jiaxuan ZhangCenter for Molecular Genetics, Institute of Translational Medicine, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao, China.
Peifeng LiCenter for Molecular Genetics, Institute of Translational Medicine, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao, China.
Jinning GaoCenter for Molecular Genetics, Institute of Translational Medicine, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao, China.
Qingdao University · CNYuxian People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patients with diabetes have severe vascular complications, such as diabetic nephropathy, diabetic retinopathy, cardiovascular disease, and neuropathy. Devastating vascular complications lead to increased mortality, blindness, kidney failure, and decreased overall quality of life in people with type 2 diabetes (T2D). Glycolipid metabolism disorder plays a vital role in the vascular complications of T2D. However, the specific mechanism of action remains to be elucidated. In T2D patients, vascular damage begins to develop before insulin resistance and clinical diagnosis. Endothelial dysregulation is a significant cause of vascular complications and the early event of vascular injury. Hyperglycemia and hyperlipidemia can trigger inflammation and oxidative stress, which impair endothelial function. Furthermore, during the pathogenesis of T2D, epigenetic modifications are aberrant and activate various biological processes, resulting in endothelial dysregulation. In the present review, we provide an overview and discussion of the roles of hyperglycemia- and hyperlipidemia-induced endothelial dysfunction, inflammatory response, oxidative stress, and epigenetic modification in the pathogenesis of T2D. Understanding the connections of glucotoxicity and lipotoxicity with vascular injury may reveal a novel potential therapeutic target for diabetic vascular complications.

Indexed as

glucose metabolismlipid metabolismT2Dtherapeutic strategyvascular injury

Identifiers

PMID36117707
PMCPMC9473659
OpenAlexW4293813126

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.