Evidence map›Paper›PMID 28800132›Full record

ArticleCell death and differentiation2017

Sphingolipid accumulation causes mitochondrial dysregulation and cell death.

Jeffrey Knupp, Fernando Martinez-Montañés, Francoise Van Den Bergh, Stephanie Cottier, Roger Schneiter, Daniel Beard, Amy Chang

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing 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

29 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Sphingolipidoses: expanding the spectrum of α-synucleinopathies.Journal of neural transmission (Vienna, Austria : 1996) · 2026
    Review
  3. Article
  4. Review
  5. Article
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  7. Article
  8. Review
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  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Mitochondrial Lipids: From Membrane Organization to Apoptotic Facilitation.International journal of molecular sciences · 2022
    Review
  17. Review
  18. Article
  19. Article
  20. The Phenoxyphenol Compound diTFPP Mediates Exogenous CAntioxidants (Basel, Switzerland) · 2021
    Article
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

7 authors at 2 institutions in 2 countries.

Jeffrey KnuppDepartment of Molecular Cellular and Developmental Biology, University of Michigan,Ann Arbor, MI, USA.
Fernando Martinez-MontañésDepartment of Biology, University of Fribourg, Fribourg, Switzerland.
Francoise Van Den BerghDepartment of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA.
Stephanie CottierDepartment of Biology, University of Fribourg, Fribourg, Switzerland.
Roger SchneiterDepartment of Biology, University of Fribourg, Fribourg, Switzerland.
Daniel BeardDepartment of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA.
Amy ChangDepartment of Molecular Cellular and Developmental Biology, University of Michigan,Ann Arbor, MI, USA.
University of Michigan–Ann Arbor · USUniversity of Fribourg · CH

Funding

Integrated Modeling of Cardiac Metabolism and TransportR01HL072011 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BEARD, DANIEL A · 2004 to 2016
$4.0M
NHLBI NIH HHS R01 HL072011
6 · The paper itself

Abstract

Sphingolipids are structural components of cell membranes that have signaling roles to regulate many activities, including mitochondrial function and cell death. Sphingolipid metabolism is integrated with numerous metabolic networks, and dysregulated sphingolipid metabolism is associated with disease. Here, we describe a monogenic yeast model for sphingolipid accumulation. A csg2Δ mutant cannot readily metabolize and accumulates the complex sphingolipid inositol phosphorylceramide (IPC). In these cells, aberrant activation of Ras GTPase is IPC-dependent, and accompanied by increased mitochondrial reactive oxygen species (ROS) and reduced mitochondrial mass. Survival or death of csg2Δ cells depends on nutritional status. Abnormal Ras activation in csg2Δ cells is associated with impaired Snf1/AMPK protein kinase, a key regulator of energy homeostasis. csg2Δ cells are rescued from ROS production and death by overexpression of mitochondrial catalase Cta1, abrogation of Ras hyperactivity or genetic activation of Snf1/AMPK. These results suggest that sphingolipid dysregulation compromises metabolic integrity via Ras and Snf1/AMPK pathways.

Indexed as

Cell DeathHumansMitochondriaReactive Oxygen SpeciesSignal TransductionSphingolipidsReactive Oxygen SpeciesSphingolipids

Identifiers

PMID28800132
PMCPMC5686345
OpenAlexW2745298720

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.