Evidence map›Paper›PMID 10229704›Full record

ReviewEnvironmental health perspectives1999

Calcium signaling and cytotoxicity.

G E Kass, S Orrenius

Open access · diamondAbstract readReview
In one paragraph

Review in Environmental health perspectives, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

70 citing papers in PubMed, 225 citations in OpenAlex.

  1. Trial
  2. Review
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  8. Article
  9. Review
  10. Logistics of Bone Mineralization in the Chick Embryo Studied by 3D Cryo FIB-SEM Imaging.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  11. Article
  12. Article
  13. Review
  14. In vitro reconstitution of calcium-dependent recruitment of the human ESCRT machinery in lysosomal membrane repair.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review

10 more citing papers are in PubMed but not listed here.

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.

G E KassSchool of Biological Sciences, University of Surrey, Guildford, United Kingdom. g.kass@surrey.ac.uk
S Orrenius
University of Surrey · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The divalent calcium cation Ca(2+) is used as a major signaling molecule during cell signal transduction to regulate energy output, cellular metabolism, and phenotype. The basis to the signaling role of Ca(2+) is an intricate network of cellular channels and transporters that allow a low resting concentration of Ca(2+) in the cytosol of the cell ([Ca(2+)]i) but that are also coupled to major dynamic and rapidly exchanging stores. This enables extracellular signals from hormones and growth factors to be transduced as [Ca(2+)]i spikes that are amplitude and frequency encoded. There is considerable evidence that a number of toxic environmental chemicals target these Ca(2+) signaling processes, alter them, and induce cell death by apoptosis. Two major pathways for apoptosis will be considered. The first one involves Ca(2+)-mediated expression of ligands that bind to and activate death receptors such as CD95 (Fas, APO-1). In the second pathway, Ca(2+) has a direct toxic effect and its primary targets include the mitochondria and the endoplasmic reticulum (ER). Mitochondria may respond to an apoptotic Ca(2+) signal by the selective release of cytochrome c or through enhanced production of reactive oxygen species and opening of an inner mitochondrial membrane pore. Toxic agents such as the environmental pollutant tributyltin or the natural plant product thapsigargin, which deplete the ER Ca(2+) stores, will induce as a direct result of this effect the opening of plasma membrane Ca(2+) channels and an ER stress response. In contrast, under some conditions, Ca(2+) signals may be cytoprotective and antagonize the apoptotic machinery.

Indexed as

ApoptosisCalcium SignalingAnimalsCalciumCell MembraneHumansMitochondriaCalcium

Identifiers

PMID10229704
PMCPMC1566353
OpenAlexW2006538087

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.