Evidence map›Paper›PMID 24111728›Full record

ReviewBritish journal of pharmacology2014

Lipid analogues as potential drugs for the regulation of mitochondrial cell death.

Michael Murray, Herryawan Ryadi Eziwar Dyari, Sarah E Allison, Tristan Rawling

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

7 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Coriolic Acid (13-(Molecules (Basel, Switzerland) · 2020
    Article
  3. Article
  4. Article
  5. Synergistic combination of alkylphosphocholines with peptaibols in targeting Leishmania infantum in vitro.International journal for parasitology. Drugs and drug resistance · 2018
    Article
  6. Cell Death and Heart Failure in Obesity: Role of Uncoupling Proteins.Oxidative medicine and cellular longevity · 2016
    Review
  7. Mitochondrial pharmacology: energy, injury and beyond.British journal of pharmacology · 2014
    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

4 authors at 2 institutions in 1 country.

Michael MurrayPharmacogenomics and Drug Development Group, Discipline of Pharmacology, University of Sydney, Sydney, NSW, Australia.
Herryawan Ryadi Eziwar Dyari
Sarah E Allison
Tristan Rawling
University of Sydney · AUUniversity of Technology Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mitochondrion plays an important role in the production of energy as ATP, the regulation of cell viability and apoptosis, and the biosynthesis of major structural and regulatory molecules, such as lipids. During ATP production, reactive oxygen species are generated that alter the intracellular redox state and activate apoptosis. Mitochondrial dysfunction is a well-recognized component of the pathogenesis of diseases such as cancer. Understanding mitochondrial function, and how this is dysregulated in disease, offers the opportunity for the development of drug molecules to specifically target such defects. Altered energy metabolism in cancer, in which ATP production occurs largely by glycolysis, rather than by oxidative phosphorylation, is attributable in part to the up-regulation of cell survival signalling cascades. These pathways also regulate the balance between pro- and anti-apoptotic factors that may determine the rate of cell death and proliferation. A number of anti-cancer drugs have been developed that target these factors and one of the most promising groups of agents in this regard are the lipid-based molecules that act directly or indirectly at the mitochondrion. These molecules have emerged in part from an understanding of the mitochondrial actions of naturally occurring fatty acids. Some of these agents have already entered clinical trials because they specifically target known mitochondrial defects in the cancer cell.

Indexed as

Adenosine TriphosphateAnticarcinogenic AgentsCell DeathEnergy MetabolismFatty AcidsLipid MetabolismMitochondriaMolecular Targeted TherapyNeoplasmsPhospholipidsAdenosine TriphosphateAnticarcinogenic AgentsFatty AcidsPhospholipidscancer cellether phospholipidsfatty acid biotransformationfree fatty acidsintrinsic pathway of apoptosismitochondrial ATP productionN-acylethanolaminespolyunsaturated fatty acid epoxidesreactive oxygen species

Identifiers

PMID24111728
PMCPMC3976621
OpenAlexW1591069210

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.