Evidence map›Paper›PMID 24445246›Full record

ReviewChemistry and physics of lipids2014

The functions of cardiolipin in cellular metabolism-potential modifiers of the Barth syndrome phenotype.

Vaishnavi Raja, Miriam L Greenberg

Abstract readReview
In one paragraph

Review in Chemistry and physics of lipids, 2014. 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
2.4field-weighted citation impact, top 11% 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, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Experimental models of Barth syndrome.Journal of inherited metabolic disease · 2022
    Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Cardiolipin-deficient cells depend on anaplerotic pathways to ameliorate defective TCA cycle function.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2019
    Article
  17. Article
  18. Article
  19. The phospholipase iPLAThe Journal of biological chemistry · 2017
    Article
  20. 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

2 authors at 1 institution in 1 country.

Vaishnavi RajaDepartment of Biological Sciences, Wayne State University, Detroit, United States.
Miriam L GreenbergDepartment of Biological Sciences, Wayne State University, Detroit, United States. Electronic address: mlgreen@sun.science.wayne.edu.
Wayne State University · US

Funding

THE ROLE OF CARDIOLIPIN IN THE TCA CYCLE: IMPLICATIONS FOR BARTH SYNDROMER01HL117880 · NHLBI · WAYNE STATE UNIVERSITY · PI GREENBERG, MIRIAM L · 2014 to 2023
$3.0M
SYNTHETIC LETHAL INTERACTIONS IN BARTH SYNDROMER21HL084218 · NHLBI · WAYNE STATE UNIVERSITY · PI GREENBERG, MIRIAM L · 2008 to 2009
$414k
NHLBI NIH HHS HL084218NHLBI NIH HHS R01 HL117880NHLBI NIH HHS R21 HL084218
6 · The paper itself

Abstract

The phospholipid cardiolipin (CL) plays a role in many cellular functions and signaling pathways both inside and outside of mitochondria. This review focuses on the role of CL in energy metabolism. Many reactions of electron transport and oxidative phosphorylation, the transport of metabolites required for these processes, and the stabilization of electron transport chain supercomplexes require CL. Recent studies indicate that CL is required for the synthesis of iron-sulfur (Fe-S) co-factors, which are essential for numerous metabolic pathways. Activation of carnitine shuttle enzymes that are required for fatty acid metabolism is CL dependent. The presence of substantial amounts of CL in the peroxisomal membrane suggests that CL may be required for peroxisomal functions. Understanding the role of CL in energy metabolism may identify physiological modifiers that exacerbate the loss of CL and underlie the variation in symptoms observed in Barth syndrome, a genetic disorder of CL metabolism.

Indexed as

PhenotypeAnimalsBarth SyndromeCardiolipinsEnergy MetabolismHomeostasisHumansMitochondriaCardiolipinsBarth syndromeBioenergeticsCarnitine transportFatty acid utilizationIron–sulfur biogenesis

Identifiers

PMID24445246
PMCPMC4342993
OpenAlexW2055203927

What OpenQuestion holds

Textmetadata
LicenceTDM
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.