Evidence map›Paper›PMID 28757580›Full record

ArticleNutrients2017

Role of Mitochondria and Endoplasmic Reticulum in Taurine-Deficiency-Mediated Apoptosis.

Chian Ju Jong, Takashi Ito, Howard Prentice, Jang-Yen Wu, Stephen W Schaffer

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

34 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
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  3. Review
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  13. A Key Metabolic Regulator of Bone and Cartilage Health.Endocrinology and metabolism (Seoul, Korea) · 2022
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Taurine in sports and exercise.Journal of the International Society of Sports Nutrition · 2021
    Review
  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

5 authors at 3 institutions in 2 countries.

Chian Ju JongDepartment of Pharmacology, College of Medicine, University of South Alabama, Mobile, AL 36688, USA. cjjong84@gmail.com.
Takashi ItoFaculty of Biotechnology, Fukui Prefectural University, Fukui 910-1195, Japan. tito@fpu.ac.jp.
Howard PrenticeProgram in Integrative Biology and Center for Complex Systems and Brain Sciences, College of Medicine, Florida Atlantic University, Boca Raton, FL 33431, USA. hprentic@health.fau.edu.
Jang-Yen WuProgram in Integrative Biology and Center for Complex Systems and Brain Sciences, College of Medicine, Florida Atlantic University, Boca Raton, FL 33431, USA. jwu@health.fau.edu.
Stephen W SchafferDepartment of Pharmacology, College of Medicine, University of South Alabama, Mobile, AL 36688, USA. sschaffe@southalabama.edu.
Florida Atlantic University · USUniversity of South Alabama · USFukui Prefectural University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Taurine is a ubiquitous sulfur-containing amino acid found in high concentration in most tissues. Because of its involvement in fundamental physiological functions, such as regulating respiratory chain activity, modulating cation transport, controlling inflammation, altering protein phosphorylation and prolonging lifespan, taurine is an important nutrient whose deficiency leads to severe pathology and cell death. However, the mechanism by which taurine deficiency causes cell death is inadequately understood. Therefore, the present study examined the hypothesis that overproduction of reactive oxygen species (ROS) by complex I of the respiratory chain triggers mitochondria-dependent apoptosis in hearts of taurine transporter knockout (TauTKO) mice. In support of the hypothesis, a 60% decrease in mitochondrial taurine content of 3-month-old TauTKO hearts was observed, which was associated with diminished complex I activity and the onset of mitochondrial oxidative stress. Oxidative damage to stressed mitochondria led to activation of a caspase cascade, with stimulation of caspases 9 and 3 prevented by treatment of 3-month-old TauTKO mice with the mitochondria specific antioxidant, MitoTempo. In 12 month-old, but not 3-month-old, TauTKO hearts, caspase 12 activation contributes to cell death, revealing a pathological role for endoplasmic reticulum (ER) stress in taurine deficient, aging mice. Thus, taurine is a cytoprotective nutrient that ensures normal mitochondrial and ER function, which is important for the reduction of risk for apoptosis and premature death.

Indexed as

ApoptosisAnimalsCaspase 12Caspase 3Caspase 9Endoplasmic ReticulumEndoplasmic Reticulum StressMembrane GlycoproteinsMembrane Transport ProteinsMiceMice, Inbred C57BLMitochondriaNADH DehydrogenaseOrganophosphorus CompoundsOxidative StressPiperidinesCasp12 protein, mouseCasp3 protein, mouseCasp9 protein, mouseCaspase 12Caspase 3Caspase 9Membrane GlycoproteinsMembrane Transport ProteinsMitoTEMPONADH DehydrogenaseNADH dehydrogenase subunit 6, mouseOrganophosphorus CompoundsPiperidinesReactive Oxygen SpeciesTaurineTaurine Transportersapoptosiscaspase cascadeendoplasmic reticulum stressmitochondriamitochondria encoded proteinsoxidative stressrespiratory chaintRNALeu(UUR)

Identifiers

PMID28757580
PMCPMC5579589
OpenAlexW2736707149

What OpenQuestion holds

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LicenceCC BY
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.