Evidence map›Paper›PMID 26515038›Full record

ArticleScientific reports2015

Deletion of Cyclophilin D Impairs β-Oxidation and Promotes Glucose Metabolism.

Michele Tavecchio, Sofia Lisanti, Michael J Bennett, Lucia R Languino, Dario C Altieri

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.5field-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

28 citing papers in PubMed, 46 citations in OpenAlex.

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  11. Mitochondrial Permeability Transition in Stem Cells, Development, and Disease.Advances in experimental medicine and biology · 2023
    Review
  12. Remodeling of Liver and Plasma Lipidomes in Mice Lacking Cyclophilin D.International journal of molecular sciences · 2022
    Article
  13. Review
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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

5 authors at 1 institution in 1 country.

Michele TavecchioProstate Cancer Discovery and Development Program, Tumor Microenvironment and Metastasis Program, The Wistar Institute, Philadelphia, PA 19104.
Sofia LisantiProstate Cancer Discovery and Development Program, Tumor Microenvironment and Metastasis Program, The Wistar Institute, Philadelphia, PA 19104.
Michael J BennettMichael Palmieri Metabolic Laboratory, Children's Hospital of Philadelphia and Department of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104.
Lucia R LanguinoDepartment of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107.
Dario C AltieriProstate Cancer Discovery and Development Program, Tumor Microenvironment and Metastasis Program, The Wistar Institute, Philadelphia, PA 19104.
Sidney Kimmel Cancer Center · US

Funding

Tumor Microenvironment and MetastasisP30CA010815 · NCI · WISTAR INSTITUTE · PI Luis J Montaner · 1985 to 2026
$75.9M
Role of Runx2 in prostate tumorigenesis and metastasisP01CA140043 · NCI · WISTAR INSTITUTE · PI ALTIERI, DARIO C · 2010 to 2021
$12.2M
CONTROL OF APOPTOSIS IN CANCER BY SURVIVINR01CA078810 · NCI · YALE UNIVERSITY · PI ALTIERI, DARIO C · 1998 to 2017
$5.5M
INTEGRIN SIGNALING PATHWAYS IN PROSTATE CANCERR01CA089720 · NCI · YALE UNIVERSITY · PI LANGUINO, LUCIA R. · 2001 to 2014
$2.8M
NCI NIH HHS CA010815NCI NIH HHS P01 CA140043NCI NIH HHS P30 CA010815NCI NIH HHS R01 CA078810NCI NIH HHS R01 CA089720NCI NIH HHS R01 CA78810PHS HHS CAA10027
6 · The paper itself

Abstract

Cyclophilin D (CypD) is a mitochondrial matrix protein implicated in cell death, but a potential role in bioenergetics is not understood. Here, we show that loss or depletion of CypD in cell lines and mice induces defects in mitochondrial bioenergetics due to impaired fatty acid β-oxidation. In turn, CypD loss triggers a global compensatory shift towards glycolysis, with transcriptional upregulation of effectors of glucose metabolism, increased glucose consumption and higher ATP production. In vivo, the glycolytic shift secondary to CypD deletion is associated with expansion of insulin-producing β-cells, mild hyperinsulinemia, improved glucose tolerance, and resistance to high fat diet-induced liver damage and weight gain. Therefore, CypD is a novel regulator of mitochondrial bioenergetics, and unexpectedly controls glucose homeostasis, in vivo.

Indexed as

Adenosine TriphosphateAnimalsBlood GlucoseCarbohydrate MetabolismCells, CulturedCholesterolCitric Acid CycleCyclophilinsDiet, High-FatFemaleGlucose Tolerance TestGlycolysisImmunohistochemistryInsulinInsulin-Secreting CellsLipid PeroxidationAdenosine TriphosphateBlood GlucoseCholesterolCyclophilinsInsulinPeptidyl-Prolyl Isomerase FPPIF protein, mouseTriglycerides

Identifiers

PMID26515038
PMCPMC4626838
OpenAlexW1859699747

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.