Evidence map›Paper›PMID 29035377›Full record

ReviewLaboratory investigation; a journal of technical methods and pathology2018

NME4/nucleoside diphosphate kinase D in cardiolipin signaling and mitophagy.

Uwe Schlattner, Malgorzata Tokarska-Schlattner, Richard M Epand, Mathieu Boissan, Marie-Lise Lacombe, Valerian E Kagan

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Laboratory investigation; a journal of technical methods and pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 17% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Guideline
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  7. Upregulation ofTranslational andrology and urology · 2026
    Article
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  18. Article
  19. Natural Products Targeting the Mitochondria in Cancers.Molecules (Basel, Switzerland) · 2020
    Review
  20. Structure, Folding and Stability of Nucleoside Diphosphate Kinases.International journal of molecular sciences · 2020
    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

6 authors at 3 institutions in 3 countries.

Uwe SchlattnerUniversity Grenoble Alpes, Inserm, Laboratory of Fundamental and Applied Bioenergetics (LBFA) and SFR Environmental and Systems Biology (BEeSy), Grenoble, France.
Malgorzata Tokarska-SchlattnerUniversity Grenoble Alpes, Inserm, Laboratory of Fundamental and Applied Bioenergetics (LBFA) and SFR Environmental and Systems Biology (BEeSy), Grenoble, France.
Richard M EpandDepartment of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON, Canada.
Mathieu BoissanSorbonne Universités, UPMC Univ Paris 06, Inserm, UMRS938, Saint-Antoine Research Center, Paris, France.
Marie-Lise LacombeSorbonne Universités, UPMC Univ Paris 06, Inserm, UMRS938, Saint-Antoine Research Center, Paris, France.
Valerian E KaganCenter for Free Radical and Antioxidant Health, Department of Environmental Health, University of Pittsburgh, Pittsburgh, PA, USA.
Inserm · FRMcMaster University · CAUniversity of Pittsburgh · US

Funding

Training and EducationU19AI068021 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GREENBERGER, JOEL S · 2005 to 2019
$44.4M
NIAID NIH HHS U19 AI068021
6 · The paper itself

Abstract

Mitophagy is an emerging paradigm for mitochondrial quality control and cell homeostasis. Dysregulation of mitophagy can lead to human pathologies such as neurodegenerative disorders and contributes to the aging process. Complex protein signaling cascades have been described that regulate mitophagy. We have identified a novel lipid signaling pathway that involves the phospholipid cardiolipin (CL). CL is synthesized and normally confined at the inner mitochondrial membrane. However, upon a mitophagic trigger, ie, collapse of the inner membrane potential, CL is rapidly externalized to the mitochondrial surface with the assistance of the hexameric nucleoside diphosphate kinase D (NME4, NDPK-D, or NM23-H4). In addition to its NDP kinase activity, NME4/NDPK-D shows intermembrane phospholipid transfer activity in vitro and in cellular systems, which relies on NME4/NDPK-D interaction with CL, CL-dependent crosslinking of inner and outer mitochondrial membranes by symmetrical, hexameric NME4/NDPK-D, and a putative NME4/NDPK-D-based CL-transfer pathway. CL exposed at the mitochondrial surface then serves as an 'eat me' signal for the mitophagic machinery; it is recognized by the LC3 receptor of autophagosomes, targeting the dysfunctional mitochondrion to lysosomal degradation. Similar NME4-supported CL externalization is likely also involved in apoptosis and inflammatory reactions.

Indexed as

MitophagySignal TransductionAnimalsApoptosisCardiolipinsHumansMitochondrial MembranesModels, BiologicalNucleoside Diphosphate Kinase DProtein BindingCardiolipinsNucleoside Diphosphate Kinase D

Identifiers

PMID29035377
OpenAlexW2766218443

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.