Evidence map›Paper›PMID 26473856›Full record

ReviewInternational journal of molecular sciences2015

Molecular Pathways Regulating Macrovascular Pathology and Vascular Smooth Muscle Cells Phenotype in Type 2 Diabetes.

Sara Casella, Alessandra Bielli, Alessandro Mauriello, Augusto Orlandi

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Extreme Diversity of the Human Vascular Mesenchymal Cell Landscape.Journal of the American Heart Association · 2020
    Pooled it
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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

4 authors at 1 institution in 1 country.

Sara CasellaDepartment of Biomedicine and Prevention, Institute of Anatomic Pathology, Tor Vergata University of Rome, Rome 00133, Italy. sara.casella87@icloud.com.
Alessandra BielliDepartment of Biomedicine and Prevention, Institute of Anatomic Pathology, Tor Vergata University of Rome, Rome 00133, Italy. alessandrabielli@hotmail.it.
Alessandro MaurielloDepartment of Biomedicine and Prevention, Institute of Anatomic Pathology, Tor Vergata University of Rome, Rome 00133, Italy. alessandro.mauriello@uniroma2.it.
Augusto OrlandiDepartment of Biomedicine and Prevention, Institute of Anatomic Pathology, Tor Vergata University of Rome, Rome 00133, Italy. orlandi@uniroma2.it.
University of Rome Tor Vergata · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 diabetes mellitus (T2DM) is a disease reaching a pandemic proportion in developed countries and a major risk factor for almost all cardiovascular diseases and their adverse clinical manifestations. T2DM leads to several macrovascular and microvascular alterations that influence the progression of cardiovascular diseases. Vascular smooth muscle cells (VSMCs) are fundamental players in macrovascular alterations of T2DM patients. VSMCs display phenotypic and functional alterations that reflect an altered intracellular biomolecular scenario of great vessels of T2DM patients. Hyperglycemia itself and through intraparietal accumulation of advanced glycation-end products (AGEs) activate different pathways, in particular nuclear factor-κB and MAPKs, while insulin and insulin growth-factor receptors (IGFR) are implicated in the activation of Akt and extracellular-signal-regulated kinases (ERK) 1/2. Nuclear factor-κB is also responsible of increased susceptibility of VSMCs to pro-apoptotic stimuli. Down-regulation of insulin growth-factor 1 receptors (IGFR-1R) activity in diabetic vessels also influences negatively miR-133a levels, so increasing apoptotic susceptibility of VSMCs. Alterations of those bimolecular pathways and related genes associate to the prevalence of a synthetic phenotype of VSMCs induces extracellular matrix alterations of great vessels. A better knowledge of those biomolecular pathways and related genes in VSMCs will help to understand the mechanisms leading to macrovascular alterations in T2DM patients and to suggest new targeted therapies.

Indexed as

ApoptosisCardiovascular DiseasesDiabetes Mellitus, Type 2Diabetic AngiopathiesExtracellular Signal-Regulated MAP KinasesGlycation End Products, AdvancedHumansHyperglycemiaInsulinMicroRNAsMuscle, Smooth, VascularMyocytes, Smooth MuscleNF-kappa BProto-Oncogene Proteins c-aktReceptor, IGF Type 1Extracellular Signal-Regulated MAP KinasesGlycation End Products, AdvancedInsulinMicroRNAsMIRN133 microRNA, humanNF-kappa BProto-Oncogene Proteins c-aktReceptor, IGF Type 1Aktapoptosisatherosclerosisdiabetesnuclear factor-κBphenotypic changes

Identifiers

PMID26473856
PMCPMC4632754
OpenAlexW2102061897

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.