Evidence map›Paper›PMID 27834824›Full record

ReviewInternational journal of molecular sciences2016

Diabetic Microvascular Disease and Pulmonary Fibrosis: The Contribution of Platelets and Systemic Inflammation.

Rekha Jagadapillai, Madhavi J Rane, Xingyu Lin, Andrew M Roberts, Gary W Hoyle, Lu Cai, Evelyne Gozal

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 5% 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, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
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  18. Observational
  19. Article
  20. Diabetic lung disease: fact or fiction?Reviews in endocrine & metabolic disorders · 2019
    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

7 authors at 2 institutions in 2 countries.

Rekha JagadapillaiDepartment of Pediatrics, School of Medicine, University of Louisville, Louisville, KY 40292, USA. rekha.jagadapillai@louisville.edu.
Madhavi J RaneMedicine/Nephrology, School of Medicine, University of Louisville, Louisville, KY 40292, USA. madhavi.rane@louisville.edu.
Xingyu LinDepartment of Pediatrics, School of Medicine, University of Louisville, Louisville, KY 40292, USA. 15943075920@163.com.
Andrew M RobertsDepartment of Pediatrics, School of Medicine, University of Louisville, Louisville, KY 40292, USA. andrew.roberts@louisville.edu.
Gary W HoyleDepartment of Environmental and Occupational Health Sciences, School of Public Health and Information Sciences, University of Louisville, Louisville, KY 40292, USA. gary.hoyle@louisville.edu.
Lu CaiDepartment of Pediatrics, School of Medicine, University of Louisville, Louisville, KY 40292, USA. lu.cai@louisville.edu.
Evelyne GozalDepartment of Pediatrics, School of Medicine, University of Louisville, Louisville, KY 40292, USA. evelyne.gozal@louisville.edu.
University of Louisville · USJilin University · CN

Funding

Metabolomics study on the preventive mechanisms for LDR on diabetic nephropathyR01DK091338 · NIDDK · UNIVERSITY OF LOUISVILLE · PI CAI, LU · 2013 to 2014
$900k
NIDDK NIH HHS R01 DK091338
6 · The paper itself

Abstract

Diabetes is strongly associated with systemic inflammation and oxidative stress, but its effect on pulmonary vascular disease and lung function has often been disregarded. Several studies identified restrictive lung disease and fibrotic changes in diabetic patients and in animal models of diabetes. While microvascular dysfunction is a well-known complication of diabetes, the mechanisms leading to diabetes-induced lung injury have largely been disregarded. We described the potential involvement of diabetes-induced platelet-endothelial interactions in perpetuating vascular inflammation and oxidative injury leading to fibrotic changes in the lung. Changes in nitric oxide synthase (NOS) activation and decreased NO bioavailability in the diabetic lung increase platelet activation and vascular injury and may account for platelet hyperreactivity reported in diabetic patients. Additionally, the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway has been reported to mediate pancreatic islet damage, and is implicated in the onset of diabetes, inflammation and vascular injury. Many growth factors and diabetes-induced agonists act via the JAK/STAT pathway. Other studies reported the contribution of the JAK/STAT pathway to the regulation of the pulmonary fibrotic process but the role of this pathway in the development of diabetic lung fibrosis has not been considered. These observations may open new therapeutic perspectives for modulating multiple pathways to mitigate diabetes onset or its pulmonary consequences.

Indexed as

AnimalsBlood PlateletsCell CommunicationDiabetes MellitusEndothelial CellsGene Expression RegulationHumansInflammationJanus Kinase 1LungNitric Oxide Synthase Type IIIOxidative StressPeripheral Vascular DiseasesPlatelet ActivationPulmonary FibrosisSignal TransductionJAK1 protein, humanJanus Kinase 1Nitric Oxide Synthase Type IIINOS3 protein, humanSTAT Transcription Factorsendothelial injuryJAK/STATlung fibrosisnitric oxideplatelet

Identifiers

PMID27834824
PMCPMC5133853
OpenAlexW2555567079

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.