Evidence map›Paper›PMID 32788622›Full record

ArticleScientific reports2020

Dysregulation of ghrelin in diabetes impairs the vascular reparative response to hindlimb ischemia in a mouse model; clinical relevance to peripheral artery disease.

Joshua P H Neale, James T Pearson, Kate N Thomas, Hirotsugu Tsuchimochi, Hiroshi Hosoda, Masayasu Kojima, Takahiro Sato, Gregory T Jones, Adam P Denny, Lorna J Daniels and 5 more

RetractedErratum issuedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 4 institutions in 3 countries.

Joshua P H NealeDepartment of Physiology, School of Biomedical Sciences and HeartOtago, University of Otago, 270 Great King Street, Dunedin, 9018, New Zealand.
James T PearsonDepartment of Cardiac Physiology, National Cerebral and Cardiovascular Center Research Institute, Suita, Osaka, Japan.
Kate N ThomasDepartment of Surgical Sciences, University of Otago, Dunedin, New Zealand.
Hirotsugu TsuchimochiDepartment of Cardiac Physiology, National Cerebral and Cardiovascular Center Research Institute, Suita, Osaka, Japan.
Hiroshi HosodaDepartment of Regenerative Medicine, National Cerebral and Cardiovascular Center Research Institute, Suita, Osaka, Japan.
Masayasu KojimaMolecular Genetics, Institute of Life Science, Kurume University, Kurume, Japan.
Takahiro SatoMolecular Genetics, Institute of Life Science, Kurume University, Kurume, Japan.
Gregory T JonesDepartment of Surgical Sciences, University of Otago, Dunedin, New Zealand.
Adam P DennyDepartment of Physiology, School of Biomedical Sciences and HeartOtago, University of Otago, 270 Great King Street, Dunedin, 9018, New Zealand.
Lorna J DanielsDepartment of Physiology, School of Biomedical Sciences and HeartOtago, University of Otago, 270 Great King Street, Dunedin, 9018, New Zealand.
Dhananjie ChandrasekeraDepartment of Physiology, School of Biomedical Sciences and HeartOtago, University of Otago, 270 Great King Street, Dunedin, 9018, New Zealand.
Ping LiuDepartment of Anatomy, School of Biomedical Sciences, University of Otago, Dunedin, New Zealand.
Andre M van RijDepartment of Surgical Sciences, University of Otago, Dunedin, New Zealand.
Rajesh Katare *Department of Physiology, School of Biomedical Sciences and HeartOtago, University of Otago, 270 Great King Street, Dunedin, 9018, New Zealand. rajesh.katare@otago.ac.nz.
Daryl O Schwenke *Department of Physiology, School of Biomedical Sciences and HeartOtago, University of Otago, 270 Great King Street, Dunedin, 9018, New Zealand. daryl.schwenke@otago.ac.nz.
University of Otago · NZKurume University · JPNational Cerebral and Cardiovascular Center · JPAustralian Regenerative Medicine Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 diabetes is a prominent risk factor for peripheral artery disease (PAD). Yet, the mechanistic link between diabetes and PAD remains unclear. This study proposes that dysregulation of the endogenous hormone ghrelin, a potent modulator of vascular function, underpins the causal link between diabetes and PAD. Moreover, this study aimed to demonstrate the therapeutic potential of exogenous ghrelin in a diabetic mouse model of PAD. Standard ELISA analysis was used to quantify and compare circulating levels of ghrelin between (i) human diabetic patients with or without PAD (clinic) and (ii) db/db diabetic and non-diabetic mice (lab). Db/db mice underwent unilateral hindlimb ischaemia (HLI) for 14 days and treated with or without exogenous ghrelin (150 µg/kg/day.) Subsequently vascular reparation, angiogenesis, hindlimb perfusion, structure and function were assessed using laser Doppler imaging, micro-CT, microangiography, and protein and micro-RNA (miRNA) analysis. We further examined hindlimb perfusion recovery of ghrelin KO mice to determine whether an impaired vascular response to HLI is linked to ghrelin dysregulation in diabetes. Patients with PAD, with or without diabetes, had significantly lower circulating levels of endogenous ghrelin, compared to healthy individuals. Diabetic db/db mice had ghrelin levels that were only 7% of non-diabetic mice. The vascular reparative capacity of diabetic db/db mice in response to HLI was impaired compared to non-diabetic mice and, importantly, comparable to ghrelin KO mice. Daily therapeutic treatment of db/db mice with ghrelin for 14 days post HLI, stimulated angiogenesis, and improved skeletal muscle architecture and cell survival, which was associated with an increase in pro-angiogenic miRNAs-126 and -132. These findings unmask an important role for endogenous ghrelin in vascular repair following limb ischemia, which appears to be downregulated in diabetic patients. Moreover, these results implicate exogenous ghrelin as a potential novel therapy to enhance perfusion in patients with lower limb PAD, especially in diabetics.

Indexed as

Disease Models, AnimalAgedAnimalsCase-Control StudiesDiabetes Mellitus, Type 2FemaleGhrelinHindlimbHumansIschemiaMaleMiceMicroRNAsMiddle AgedNeovascularization, PathologicPeripheral Arterial DiseaseGhrelinMicroRNAs

Identifiers

PMID32788622
PMCPMC7423620
OpenAlexW3048824658

What OpenQuestion holds

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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.