Evidence map›Paper›PMID 17876565›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2008

Inhibitory effects of fenofibrate on apoptosis and cell proliferation in human endothelial cells in high glucose.

Michela Zanetti, Alessia Stocca, Barbara Dapas, Rossella Farra, Laura Uxa, Alessandra Bosutti, Rocco Barazzoni, Fleur Bossi, Carlo Giansante, Francesco Tedesco and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

19 citing papers in PubMed, 45 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

13 authors at 3 institutions in 1 country.

Michela ZanettiUCO Clinica Medica-DSCMT, Ospedale di Cattinara, Strada di Fiume 447, 34100, Trieste, Italy. zanetti@units.it
Alessia Stocca
Barbara Dapas
Rossella Farra
Laura Uxa
Alessandra Bosutti
Rocco Barazzoni
Fleur Bossi
Carlo Giansante
Francesco Tedesco
Luigi Cattin
Gianfranco Guarnieri
Gabriele Grassi
Ospedale di Cattinara · ITUniversity of Trieste · ITAzienda Sanitaria Universitaria Integrata di Trieste · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fenofibrate has beneficial effects on the progression and clinical emergence of atherosclerosis in normoglycemic and in diabetic patients. Given the involvement of endothelium in these processes, we speculated that fenofibrate may influence endothelial cell apoptosis and proliferation, regulators of endothelium integrity. Fenofibrate effects on apoptosis and proliferation were studied in human umbilical vein endothelial cells under normal (5.5 mmol/l, NG) and high (22 mmol/l, HG) glucose with or without fenofibrate (50 micromol/l). Apoptosis was evaluated by annexin V, by poly(ADP-ribose) polymerase protein cleavage, and cyclooxygenase-2 (COX-2), Bax/Bcl-2, and p53 protein levels; proliferation was assessed by determining cell cycle phase distribution and the amounts of the cell cycle regulators E2F1, cyclin D1, E1, and A and the levels of the hyper-phosphorylated form of the retinoblastoma protein (ppRb). HG resulted in increased (p<0.05) apoptosis rate associated with COX-2 protein overexpression, without modification of Bax/Bcl2 ratio and p53 levels. Fenofibrate decreased apoptosis and normalized increased COX-2 expression in HG (p<0.05). Both in HG and NG, fenofibrate dramatically reduced cell proliferation (p<0.05) through a G1/G0 block mediated by the reduction in ppRb and the decrease in E2F1, cyclin E1, A, and D1 protein expression, with a mechanism that, for cyclin E1, occurred at the posttranscriptional level. In conclusion, our data show that fenofibrate reduces apoptosis caused by HG but severely interferes with endothelial cell proliferation both in NG and HG. The resulting effect may influence endothelium integrity in vivo and may impact the outcome of acute complications of atherosclerosis in diabetes.

Indexed as

Apoptosisbcl-2-Associated X ProteinCell CycleCell ProliferationCells, CulturedCell SurvivalCyclin ACyclin DCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Cyclin ECyclinsCyclooxygenase 2Dose-Response Relationship, DrugE2F1 Transcription FactorEndothelial CellsBAX protein, humanbcl-2-Associated X ProteinCCNE1 protein, humanCDKN1A protein, humanCDKN1B protein, humanCyclin ACyclin DCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Cyclin ECyclinsCyclooxygenase 2E2F1 protein, humanE2F1 Transcription FactorFenofibrateGlucoseHypolipidemic AgentsIntracellular Signaling Peptides and ProteinsOncogene ProteinsPPAR alphaProto-Oncogene Proteins c-bcl-2PTGS2 protein, humanRetinoblastoma ProteinSuperoxidesTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID17876565
OpenAlexW2145567871

What OpenQuestion holds

Textmetadata
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.