Evidence map›Paper›PMID 29253812›Full record

ArticleRedox biology2018

Short-term sustained hyperglycaemia fosters an archetypal senescence-associated secretory phenotype in endothelial cells and macrophages.

Francesco Prattichizzo, Valeria De Nigris, Elettra Mancuso, Rosangela Spiga, Angelica Giuliani, Giulia Matacchione, Raffaella Lazzarini, Fiorella Marcheselli, Rina Recchioni, Roberto Testa and 5 more

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed, 2 pooled it
6.7field-weighted citation impact, top 3% 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

101 citing papers in PubMed, 2 syntheses or guidelines pooled it, 152 citations in OpenAlex.

  1. Pooled it
  2. Type 2 Diabetes: How Much of an Autoimmune Disease?Frontiers in endocrinology · 2019
    Pooled it
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41 more citing papers are in PubMed but not listed here.

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

15 authors at 6 institutions in 2 countries.

Francesco PrattichizzoIRCCS MultiMedica, Sesto San Giovanni,Milano, Italy; Diabetes and Obesity Research Laboratory, Institut d'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), Barcelona, Spain. Electronic address: f.prattichizzo@univpm.it.
Valeria De NigrisDiabetes and Obesity Research Laboratory, Institut d'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), Barcelona, Spain; CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Spain.
Elettra MancusoDiabetes and Obesity Research Laboratory, Institut d'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), Barcelona, Spain; Department of Medical and Surgical Sciences, Viale Europa, University Magna-Græcia of Catanzaro, Italy.
Rosangela SpigaDiabetes and Obesity Research Laboratory, Institut d'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), Barcelona, Spain; Department of Medical and Surgical Sciences, Viale Europa, University Magna-Græcia of Catanzaro, Italy.
Angelica GiulianiDepartment of Clinical and Molecular Sciences, DISCLIMO, Università Politecnica delle Marche, Ancona, Italy.
Giulia MatacchioneDepartment of Clinical and Molecular Sciences, DISCLIMO, Università Politecnica delle Marche, Ancona, Italy.
Raffaella LazzariniDepartment of Molecular and Clinical Sciences - Histology, Marche Polytechnic University, Ancona, Italy.
Fiorella MarcheselliCenter of Clinical Pathology and Innovative Therapy, INRCA-IRCCS National Institute, Ancona, Italy.
Rina RecchioniCenter of Clinical Pathology and Innovative Therapy, INRCA-IRCCS National Institute, Ancona, Italy.
Roberto TestaClinical Laboratory and Molecular Diagnostics, INRCA-IRCCS National Institute, Ancona, Italy.
Lucia La SalaIRCCS MultiMedica, Sesto San Giovanni,Milano, Italy.
Maria Rita RippoDepartment of Clinical and Molecular Sciences, DISCLIMO, Università Politecnica delle Marche, Ancona, Italy.
Antonio Domenico ProcopioDepartment of Clinical and Molecular Sciences, DISCLIMO, Università Politecnica delle Marche, Ancona, Italy; Center of Clinical Pathology and Innovative Therapy, INRCA-IRCCS National Institute, Ancona, Italy.
Fabiola OlivieriDepartment of Clinical and Molecular Sciences, DISCLIMO, Università Politecnica delle Marche, Ancona, Italy; Center of Clinical Pathology and Innovative Therapy, INRCA-IRCCS National Institute, Ancona, Italy.
Antonio CerielloDiabetes and Obesity Research Laboratory, Institut d'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), Barcelona, Spain; CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Spain; Department of Cardiovascular and Metabolic Diseases, IRCCS Multimedica, Sesto San Giovanni, Milano, Italy.
Marche Polytechnic University · ITIstituto Nazionale di Riposo e Cura per Anziani · ITCentro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas · ESMagna Graecia University · ITConsorci Institut D'Investigacions Biomediques August Pi I Sunyer · ESMultiMedica · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic status is characterized by chronic low-grade inflammation and an increased burden of senescent cells. Recently, the senescence-associated secretory phenotype (SASP) has been suggested as a possible source of inflammatory factors in obesity-induced type 2 diabetes. However, while senescence is a known consequence of hyperglycaemia, evidences of SASP as a result of the glycaemic insult are missing. In addition, few data are available regarding which cell types are the main SASP-spreading cells in vivo. Adopting a four-pronged approach we demonstrated that: i) an archetypal SASP response that was at least partly attributable to endothelial cells and macrophages is induced in mouse kidney after in vivo exposure to sustained hyperglycaemia; ii) reproducing a similar condition in vitro in endothelial cells and macrophages, hyperglycaemic stimulus largely phenocopies the SASP acquired during replicative senescence; iii) in endothelial cells, hyperglycaemia-induced senescence and SASP could be prevented by SOD-1 overexpression; and iiii) ex vivo circulating angiogenic cells derived from peripheral blood mononuclear cells from diabetic patients displayed features consistent with the SASP. Overall, the present findings document a direct link between hyperglycaemia and the SASP in endothelial cells and macrophages, making the SASP a highly likely contributor to the fuelling of low-grade inflammation in diabetes.

Indexed as

AnimalsCellular SenescenceDiabetes Mellitus, Type 2Endothelial CellsFibroblastsGene Expression RegulationHumansHyperglycemiaInflammationKidneyLeukocytes, MononuclearMacrophagesMicePhenotypeSuperoxide Dismutase-1Sod1 protein, mouseSuperoxide Dismutase-1Anion superoxideDiabetesEndothelial cellsInflammationMacrophagesSenescence associated secretory phenotype

Identifiers

PMID29253812
PMCPMC5735298
OpenAlexW2773411682

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.