Evidence map›Paper›PMID 35528840›Full record

ArticleFrontiers in cardiovascular medicine2022

Circulating Exosomal miR-181b-5p Promoted Cell Senescence and Inhibited Angiogenesis to Impair Diabetic Foot Ulcer via the Nuclear Factor Erythroid 2-Related Factor 2/Heme Oxygenase-1 Pathway.

Shaohua Wang, Min Shi, Jing Zhou, Wenjing Wang, Yuanyuan Zhang, Yongjun Li

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

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  10. Targeting Signalling Pathways in Chronic Wound Healing.International journal of molecular sciences · 2023
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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

6 authors at 2 institutions in 1 country.

Shaohua WangHebei Key Laboratory of Laboratory Medicine, Department of Clinical Laboratory, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Min ShiHebei Key Laboratory of Laboratory Medicine, Department of Clinical Laboratory, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Jing ZhouDepartment of Endocrinology, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Wenjing WangHebei Key Laboratory of Laboratory Medicine, Department of Clinical Laboratory, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Yuanyuan ZhangHebei Key Laboratory of Laboratory Medicine, Department of Clinical Laboratory, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Yongjun LiHebei Key Laboratory of Laboratory Medicine, Department of Clinical Laboratory, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Second Hospital of Hebei Medical University · CNHebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial cell dysfunction is the main contributing factor of diabetic foot ulcer (DFU). Circulating exosomes have been found to play an important role in many processes, such as cell senescence and angiogenesis. However, the underlying roles and mechanism of circulating exosomes in the onset and progression of DFU remain unclear. In this study, we isolated exosomes from the plasma of patients with DFU (DFU-Exos) and non-diabetic foot wounds (NDF-Exos). DFU-Exos promoted cell senescence and inhibited tube formation in Human Umbilical Vein Endothelial Cells (HUVECs), unlike NDF-Exos. Several datasets suggest that miR-181b-5p expression might be enriched in exosomes from DFU; this was verified using quantitative real-time PCR (qRT-PCR). We also found that miR-181b-5p, which was taken up by HUVECs, promoted cell senescence and inhibited tube formation. Dual luciferase reporter assay, qRT-PCR, Western blotting, and immunofluorescence staining confirmed that miR-181b-5p could negatively regulate nuclear factor erythroid 2-related factor 2 (NRF2) expression by binding to its 3' UTR, thus further suppressing heme oxygenase-1 (HO-1) expression. In addition, NRF2 and HO-1 inhibitors could also rescue the effects of senescence and tube formation exerted by miR-181b-5p inhibitor.

Indexed as

angiogenesisdiabetic foot ulcerexosomesmiR-181b-5psenescence (leaf)

Identifiers

PMID35528840
PMCPMC9067436
OpenAlexW4224295989

What OpenQuestion 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 OpenQuestion graph.