Evidence map›Paper›PMID 35091448›Full record

Observational studyBMJ open diabetes research & care2022

Extracellular Hsp90α, which participates in vascular inflammation, is a novel serum predictor of atherosclerosis in type 2 diabetes.

Xinyi Ding, Chuzhen Meng, Hangming Dong, Shili Zhang, Hui Zhou, Wenchong Tan, Lei Huang, Aiping He, Jieyou Li, Jiali Huang and 3 more

Registry-linked trialOpen access · goldAbstract readObservational Study
In one paragraph

Observational study in BMJ open diabetes research & care, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04787770 (The Role of HSP90 in Peripheral Vascular Lesions of Diabetic Atherosclerosis), which is not on this map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.2field-weighted citation impact, top 12% 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.

NCT04787770 completednot on this map

The Role of HSP90 in Peripheral Vascular Lesions of Diabetic Atherosclerosis

TypeobservationalSponsorNanfang Hospital, Southern Medical UniversityRan2020 to 2020Enrolled150ConditionsPeripheral Arterial DiseaseArmsnon-intervention
3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 28 citations in OpenAlex.

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  9. Investigating the Mechanisms ofFood science & nutrition · 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

13 authors at 3 institutions in 2 countries.

Xinyi Ding *Department of Occupational Health and Medicine, Southern Medical University, Guangzhou, Guangdong, China.
Chuzhen Meng *Department of Endocrinology and Metabolism, Southern Medical University Nanfang Hospital, Guangzhou, Guangdong, China.
Hangming Dong *Department of Respiratory and Critical Care Medicine, Southern Medical University Nanfang Hospital, Guangzhou, Guangdong, China.
Shili ZhangDepartment of Endocrinology and Metabolism, Southern Medical University Nanfang Hospital, Guangzhou, Guangdong, China.
Hui ZhouDepartment of Occupational Health and Medicine, Southern Medical University, Guangzhou, Guangdong, China.
Wenchong TanDepartment of Occupational Health and Medicine, Southern Medical University, Guangzhou, Guangdong, China.
Lei HuangDepartment of Burns, Southern Medical University Nanfang Hospital, Guangzhou, Guangdong, China.
Aiping HeDepartment of Endocrinology and Metabolism, Southern Medical University Nanfang Hospital, Guangzhou, Guangdong, China.
Jieyou LiDepartment of Occupational Health and Medicine, Southern Medical University, Guangzhou, Guangdong, China.
Jiali HuangDepartment of Endocrinology and Metabolism, Southern Medical University Nanfang Hospital, Guangzhou, Guangdong, China.
Wei LiDepartment of Dermatology and the Norris Comprehensive Cancer Center, Keck Medical Centre, University of Southern California, Los Angeles, California, USA zoumc163@163.com zfei@smu.edu.cn wli@usc.edu.
Fei ZouDepartment of Occupational Health and Medicine, Southern Medical University, Guangzhou, Guangdong, China zoumc163@163.com zfei@smu.edu.cn wli@usc.edu.
MengChen ZouDepartment of Endocrinology and Metabolism, Southern Medical University Nanfang Hospital, Guangzhou, Guangdong, China zoumc163@163.com zfei@smu.edu.cn wli@usc.edu.ORCID 0000-0003-1409-4645
Nanfang Hospital · CNSouthern Medical University · CNUniversity of Southern California · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAtherosclerosis is the main pathological change in diabetic angiopathy, and vascular inflammation plays an important role in early atherosclerosis. Extracellular heat shock protein 90 (eHsp90) is secreted into the serum and is involved in various physiological and pathophysiological processes. However, the specific mechanism of eHsp90 in early atherosclerosis remains unclear. This study explored the relationship between Hsp90 and diabetic lower extremity arterial disease and investigated the expression of eHsp90 in vascular endothelial cells under environmental stimulation and the function and mechanism of eHsp90α involved in diabetic atherosclerosis. RESEARCH DESIGN AND

methodsOne hundred and three selected patients were divided into three groups: the diabetes mellitus group (n=27), the diabetic lower extremity arterial disease group (n=46), and the diabetic critical limb ischemia group (n=30). The relationships among serum Hsp90, oxidative stress indexes, and patient outcomes and the correlations among the indexes were analyzed. H&E staining and immunohistochemistry were used to observe the vasculature of amputated feet from patients with diabetic foot. An oxidative stress endothelial injury model was established under high glucose in vitro to explore the role of eHsp90 release in atherosclerosis progression.

resultsThe level of serum Hsp90 was upregulated with aggravation of diabetic vascular disease. Hsp90α was correlated with malondialdehyde to some extent and was an independent risk factor in the progression of diabetic vascular disease, with predictive ability. The expression area of Hsp90α was consistent with the area of inflammatory infiltration in the vessel lumen. Vascular endothelial cells were found to increase eHsp90α secretion under stress. Then inhibition of eHsp90α can reduce the degree of cellular inflammation and damage. Endothelial cell-conditioned medium and recombinant human Hsp90α increased monocyte migration via the low-denisity lipoprotein receptor-related protein 1 (LRP1) receptor to promote disease progression.

conclusionseHsp90α plays a critical role in the early inflammatory injury stage of atherosclerosis. TRIAL REGISTRATION NUMBER: NCT04787770.

Indexed as

AtherosclerosisDiabetes Mellitus, Type 2Endothelial CellsHSP90 Heat-Shock ProteinsHumansInflammationHSP90 Heat-Shock Proteinsatherosclerosisdiabetes mellitusearly diagnosistype 2vascular

Identifiers

PMID35091448
PMCPMC8804642
OpenAlexW4210263104

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

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.