Evidence map›Paper›PMID 33050121›Full record

ArticleInternational journal of molecular sciences2020

Role of TSPO/VDAC1 Upregulation and Matrix Metalloproteinase-2 Localization in the Dysfunctional Myocardium of Hyperglycaemic Rats.

Micaela Gliozzi, Federica Scarano, Vincenzo Musolino, Cristina Carresi, Miriam Scicchitano, Stefano Ruga, Maria Caterina Zito, Saverio Nucera, Francesca Bosco, Jessica Maiuolo and 9 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-weighted citation impact, top 18% 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, 17 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Doxycycline Decreases Atherosclerotic Lesions in the Aorta ofInternational journal of molecular sciences · 2022
    Article
  5. Review
  6. Review
  7. Molecules (Basel, Switzerland) · 2020
    Review
  8. Article
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

19 authors at 2 institutions in 1 country.

Micaela GliozziIRC-FSH Department of Health Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.
Federica ScaranoIRC-FSH Department of Health Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.
Vincenzo MusolinoIRC-FSH Department of Health Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.
Cristina CarresiIRC-FSH Department of Health Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.
Miriam ScicchitanoIRC-FSH Department of Health Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.
Stefano RugaIRC-FSH Department of Health Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.
Maria Caterina ZitoIRC-FSH Department of Health Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.
Saverio NuceraIRC-FSH Department of Health Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.
Francesca BoscoIRC-FSH Department of Health Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.
Jessica MaiuoloIRC-FSH Department of Health Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.
Roberta MacrìIRC-FSH Department of Health Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.
Lorenza GuarnieriIRC-FSH Department of Health Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.
Rocco MollaceIRC-FSH Department of Health Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.ORCID 0000-0002-7106-5595
Anna Rita CoppolettaIRC-FSH Department of Health Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.
Caterina NicitaIRC-FSH Department of Health Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.
Annamaria TaverneseRenato Dulbecco Institute, Presso Fondazione Terina, 88046 Lamezia Terme (CZ), Italy.
Ernesto PalmaIRC-FSH Department of Health Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.ORCID 0000-0003-4199-207X
Carolina MuscoliIRC-FSH Department of Health Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.
Vincenzo MollaceIRC-FSH Department of Health Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.
Magna Graecia University · ITPoliclinico Tor Vergata · IT

Funding

Ministero dell'Istruzione, dell'Università e della Ricerca PON03PE_00078_1 and PON03PE_00078_2
6 · The paper itself

Abstract

Clinical management of diabetic cardiomyopathy represents an unmet need owing to insufficient knowledge about the molecular mechanisms underlying the dysfunctional heart. The aim of this work is to better clarify the role of matrix metalloproteinase 2 (MMP-2) isoforms and of translocator protein (TSPO)/voltage-dependent anion-selective channel 1 (VDAC1) modulation in the development of hyperglycaemia-induced myocardial injury. Hyperglycaemia was induced in Sprague-Dawley rats through a streptozocin injection (35 mg/Kg, i.p.). After 60 days, cardiac function was analysed by echocardiography. Nicotinamide Adenine Dinucleotide Phosphate NADPH oxidase and TSPO expression was assessed by immunohistochemistry. MMP-2 activity was detected by zymography. Superoxide anion production was estimated by MitoSOX™ staining. Voltage-dependent anion-selective channel 1 (VDAC-1), B-cell lymphoma 2 (Bcl-2), and cytochrome C expression was assessed by Western blot. Hyperglycaemic rats displayed cardiac dysfunction; this response was characterized by an overexpression of NADPH oxidase, accompanied by an increase of superoxide anion production. Under hyperglycaemia, increased expression of TSPO and VDAC1 was detected. MMP-2 downregulated activity occurred under hyperglycemia and this profile of activation was accompanied by the translocation of intracellular N-terminal truncated isoform of MMP-2 (NT-MMP-2) from mitochondria-associated membrane (MAM) into mitochondria. In the onset of diabetic cardiomyopathy, mitochondrial impairment in cardiomyocytes is characterized by the dysregulation of the different MMP-2 isoforms. This can imply the generation of a "frail" myocardial tissue unable to adapt itself to stress.

Indexed as

Disease SusceptibilityAnimalsBiomarkersCardiomyopathiesCarrier ProteinsHyperglycemiaIsoenzymesMatrix Metalloproteinase 2Models, BiologicalMyocardial ContractionNADPH OxidasesProtein BindingProtein TransportRatsReceptors, GABA-AVentricular DysfunctionBiomarkersCarrier ProteinsIsoenzymesMatrix Metalloproteinase 2NADPH OxidasesReceptors, GABA-ATspo protein, ratVdac1 protein, ratVoltage-Dependent Anion Channel 1cardiomyocytediabeteshyperglycaemiaMAMmitochondrial dysfunctionMMP-2myocardiumsuperoxide anionTSPOVDAC1

Identifiers

PMID33050121
PMCPMC7587933
OpenAlexW3091818688

What Socratic 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 Socratic graph.