Evidence map›Paper›PMID 39493878›Full record

ArticleiScience2024

Exploring heparin's protective mechanism against AGEs induced endothelial injury.

Junfeng Shi, Yudong Guan, Hongwei Song, Liang Zhu, Jingjing Li, Qinying Li, Ningning Hou, Fang Han, Meng Wang, Kexin Zhang and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

13 authors.

Junfeng ShiDepartment of Endocrinology and Metabolism, Affiliated Hospital of Shandong Second Medical University, Weifang, China.
Yudong GuanSchool of Stomatology, Henan University, Kaifeng, Henan, China.
Hongwei SongDepartment of Endocrinology and Metabolism, Affiliated Hospital of Shandong Second Medical University, Weifang, China.
Liang ZhuDepartment of Endocrinology and Metabolism, Affiliated Hospital of Shandong Second Medical University, Weifang, China.
Jingjing LiDepartment of Oncology, Affiliated Hospital of Shandong Second Medical University, Weifang, China.
Qinying LiDepartment of Endocrinology and Metabolism, Affiliated Hospital of Shandong Second Medical University, Weifang, China.
Ningning HouDepartment of Endocrinology and Metabolism, Affiliated Hospital of Shandong Second Medical University, Weifang, China.
Fang HanDepartment of Endocrinology and Metabolism, Affiliated Hospital of Shandong Second Medical University, Weifang, China.
Meng WangDepartment of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Shandong Second Medical University, Weifang, China.
Kexin ZhangDepartment of Endocrinology and Metabolism, Affiliated Hospital of Shandong Second Medical University, Weifang, China.
Ming ShanMedical Research Center, The Affiliated Hospital of Qingdao University, 16 Jiangsu Road, Qingdao, P.R. China.
Xiaodong SunDepartment of Endocrinology and Metabolism, Affiliated Hospital of Shandong Second Medical University, Weifang, China.
Hongyan QiuDepartment of Endocrinology and Metabolism, Affiliated Hospital of Shandong Second Medical University, Weifang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Advanced glycation end products (AGEs) in diabetes can cause endothelial damage. Heparin, widely known as a recognized anticoagulant, is also a multifunctional therapeutic drug. This study investigated whether heparin could ameliorate AGEs-induced endothelial injury. Remarkably, heparin effectively attenuated this cellular damage and assumed a reparative role. Furthermore, heparin inhibited the AGEs-RAGE-NFκB axis, thereby mitigating endothelial inflammatory injury. Comprehensive proteome and knockdown experiments suggested that heparin may exert a positive influence on cell growth and further alleviate pathological damage by upregulating the expression of LYAR (cell growth-regulating nucleolar protein). Diabetic mouse model was also used to further verify the changes of endothelial tissue in diabetic state and heparin intervention. In summary, these findings demonstrate that heparin has the potential to ameliorate AGEs-induced endothelial injury, opening new avenues for exploring the expanded therapeutic roles of heparin and its potential application in the management of diabetes and its associated complications.

Indexed as

Cell biologyEndocrine system physiologyHuman metabolism

Identifiers

PMID39493878
PMCPMC11530820

What OpenQuestion holds

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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.