Evidence map›Paper›PMID 25082152›Full record

ReviewJournal of leukocyte biology2014

A river runs through it: how autophagy, senescence, and phagocytosis could be linked to phospholipase D by Wnt signaling.

Julian Gomez-Cambronero, Samuel Kantonen

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of leukocyte biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Senescence of Alveolar Type 2 Cells Drives Progressive Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2021
    Article
  6. D-series Resolvins activate Phospholipase D in phagocytes during inflammation and resolution.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  7. Article
  8. Review
  9. Activation of the miR-34a-Mediated SIRT1/mTOR Signaling Pathway by Urolithin A Attenuates D-Galactose-Induced Brain Aging in Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Wnt/β-catenin signaling in kidney injury and repair: a double-edged sword.Laboratory investigation; a journal of technical methods and pathology · 2016
    Review
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

2 authors at 1 institution in 1 country.

Julian Gomez-CambroneroWright State University School of Medicine, Department of Biochemistry and Molecular Biology, Dayton, Ohio, USA julian.cambronero@wright.edu.
Samuel KantonenWright State University School of Medicine, Department of Biochemistry and Molecular Biology, Dayton, Ohio, USA.
Wright State University · US

Funding

PLD2, as a GEF or as a Lipase, is Central to Leukocyte ChemotaxisR01HL056653 · NHLBI · WRIGHT STATE UNIVERSITY · PI CAMBRONERO, JULIAN G. · 2004 to 2016
$4.0M
SIGNAL TRANSDUCTION IN NEUTROPHIL MEDIATED HEART INJURYR29HL056653 · NHLBI · WRIGHT STATE UNIVERSITY · PI GOMEZ-CAMBRONERO, JULIAN · 1998 to 2002
$301k
NHLBI NIH HHS HL056653-14NHLBI NIH HHS R01 HL056653NHLBI NIH HHS R29 HL056653
6 · The paper itself

Abstract

Neutrophils and macrophages are professional phagocytic cells, extremely efficient at the process of engulfing and killing bacteria. Autophagy is a similar process, by which phagosomes recycle internal cell structures during nutrient shortages. Some pathogens are able to subvert the autophagy process, funneling nutrients for their own use and for the host's detriment. Additionally, a failure to mount an efficient autophagy is a deviation on the cell's part from normal cellular function into cell senescence and cessation of the cell cycle. In spite of these reasons, the mechanism of autophagy and senescence in leukocytes has been under studied. We advance here the concept of a common thread underlying both autophagy and senescence, which implicates PLD. Such a PLD-based autophagy mechanism would involve two positive inputs: the generation of PA to help the initiation of the autophagosome and a protein-protein interaction between PLD and PKC that leads to enhanced PA. One negative input is also involved in this process: down-regulation of PLD gene expression by mTOR. Additionally, a dual positive/negative input plays a role in PLD-mediated autophagy, β-catenin increase of autophagy through PLD up-regulation, and a subsequent feedback termination by Dvl degradation in case of excessive autophagy. An abnormal PLD-mTOR-PKC-β-catenin/Wnt network function could lead to faulty autophagy and a means for opportunistic pathogens to survive inside of the cell.

Indexed as

Wnt Signaling PathwayAnimalsAutophagyCellular SenescenceHost-Pathogen InteractionsHumansLeukocytesPhagocytesPhagocytosisPhagosomesPhospholipase DPhospholipase Dcancercatabolic metabolismcell survivalinflammationmTORorganogenesis

Identifiers

PMID25082152
PMCPMC4197569
OpenAlexW2135086572

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.