Evidence map›Paper›PMID 26788246›Full record

ArticleOxidative medicine and cellular longevity2016

Maladaptive Modulations of NLRP3 Inflammasome and Cardioprotective Pathways Are Involved in Diet-Induced Exacerbation of Myocardial Ischemia/Reperfusion Injury in Mice.

Raffaella Mastrocola, Massimo Collino, Claudia Penna, Debora Nigro, Fausto Chiazza, Veronica Fracasso, Francesca Tullio, Giuseppe Alloatti, Pasquale Pagliaro, Manuela Aragno

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 2 pooled it
4.0field-weighted citation impact, top 6% 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

37 citing papers in PubMed, 2 syntheses or guidelines pooled it, 65 citations in OpenAlex.

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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

10 authors at 2 institutions in 1 country.

Raffaella MastrocolaDepartment of Clinical and Biological Sciences, University of Turin, Regione Gonzole 10, Orbassano, 10043 Torino, Italy.ORCID 0000-0002-0104-6129
Massimo CollinoDepartment of Drug Science and Technology, University of Turin, Corso Raffaello 33, 10125 Torino, Italy.ORCID 0000-0001-8782-3496
Claudia PennaDepartment of Clinical and Biological Sciences, University of Turin, Regione Gonzole 10, Orbassano, 10043 Torino, Italy.
Debora NigroDepartment of Clinical and Biological Sciences, University of Turin, Regione Gonzole 10, Orbassano, 10043 Torino, Italy.
Fausto ChiazzaDepartment of Drug Science and Technology, University of Turin, Corso Raffaello 33, 10125 Torino, Italy.
Veronica FracassoDepartment of Clinical and Biological Sciences, University of Turin, Regione Gonzole 10, Orbassano, 10043 Torino, Italy.
Francesca TullioDepartment of Clinical and Biological Sciences, University of Turin, Regione Gonzole 10, Orbassano, 10043 Torino, Italy.
Giuseppe AlloattiDepartment of Life Sciences and Systems Biology, University of Torino, via Accademia Albertina 13, 10123 Torino, Italy; National Institute for Cardiovascular Research, via Irnerio 48, 40126 Bologna, Italy.ORCID 0000-0003-4147-159X
Pasquale PagliaroDepartment of Clinical and Biological Sciences, University of Turin, Regione Gonzole 10, Orbassano, 10043 Torino, Italy.ORCID 0000-0002-4386-1383
Manuela AragnoDepartment of Clinical and Biological Sciences, University of Turin, Regione Gonzole 10, Orbassano, 10043 Torino, Italy.
University of Turin · ITAccademia Albertina delle Belle Arti · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive fatty acids and sugars intake is known to affect the development of cardiovascular diseases, including myocardial infarction. However, the underlying mechanisms are ill defined. Here we investigated the balance between prosurvival and detrimental pathways within the heart of C57Bl/6 male mice fed a standard diet (SD) or a high-fat high-fructose diet (HFHF) for 12 weeks and exposed to cardiac ex vivo ischemia/reperfusion (IR) injury. Dietary manipulation evokes a maladaptive response in heart mice, as demonstrated by the shift of myosin heavy chain isoform content from α to β, the increased expression of the Nlrp3 inflammasome and markers of oxidative metabolism, and the downregulation of the hypoxia inducible factor- (HIF-)2α and members of the Reperfusion Injury Salvage Kinases (RISK) pathway. When exposed to IR, HFHF mice hearts showed greater infarct size and lactic dehydrogenase release in comparison with SD mice. These effects were associated with an exacerbated overexpression of Nlrp3 inflammasome, resulting in marked caspase-1 activation and a compromised activation of the cardioprotective RISK/HIF-2α pathways. The common mechanisms of damage here reported lead to a better understanding of the cross-talk among prosurvival and detrimental pathways leading to the development of cardiovascular disorders associated with metabolic diseases.

Indexed as

Disease ProgressionAnimalsBlotting, WesternCardiotonic AgentsCarrier ProteinsCell SurvivalDietDiet, High-FatGlucose Transporter Type 4InflammasomesInsulin Receptor Substrate ProteinsLipid PeroxidationL-Lactate DehydrogenaseMaleMice, Inbred C57BLMitochondriaCardiotonic AgentsCarrier ProteinsGlucose Transporter Type 4HIF-2 protein, mouseInflammasomesInsulin Receptor Substrate ProteinsIrs2 protein, mouseL-Lactate DehydrogenaseNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseTranscription Factors

Identifiers

PMID26788246
PMCPMC4691622
OpenAlexW1841438821

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.