Evidence map›Paper›PMID 16685598›Full record

ReviewThe Journal of membrane biology2006

Volume-sensitive chloride channels involved in apoptotic volume decrease and cell death.

Y Okada, T Shimizu, E Maeno, S Tanabe, X Wang, N Takahashi

Abstract readReview
PubMed Publisher
In one paragraph

Review in The Journal of membrane biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

99 citing papers in PubMed, 229 citations in OpenAlex.

  1. Review
  2. Article
  3. Cholesterol regulation of mechanosensitive ion channels.Frontiers in cell and developmental biology · 2024
    Review
  4. Review
  5. Apoptotic volume decrease (AVD) in AFrontiers in physiology · 2023
    Article
  6. Review
  7. Article
  8. Article
  9. Mechanisms Underlying Influence of Bioelectricity in Development.Frontiers in cell and developmental biology · 2022
    Review
  10. The Important Role of Ion Transport System in Cervical Cancer.International journal of molecular sciences · 2021
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Acid- and Volume-Sensitive Chloride Currents in Human Chondrocytes.Frontiers in cell and developmental biology · 2020
    Article
  17. A Reverse-Osmosis Model of Apoptotic Shrinkage.Frontiers in cell and developmental biology · 2020
    Article
  18. Review
  19. CaFrontiers in cell and developmental biology · 2020
    Article
  20. Ions, the Movement of Water and the Apoptotic Volume Decrease.Frontiers in cell and developmental biology · 2020
    Review

39 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

6 authors at 1 institution in 1 country.

Y OkadaDepartment of Cell Physiology, National Institute for Physiological Sciences, Okazaki 444-8585, Japan. okada@nips.ac.jp
T Shimizu
E Maeno
S Tanabe
X Wang
N Takahashi
National Institute for Physiological Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apoptosis is an essential process in organ development, tissue homeostasis, somatic cell turnover, and the pathogenesis of degenerative diseases. Apoptotic cell death occurs in response to a variety of stimuli in physiological and pathological circumstances. Efflux of K(+) and Cl(-) leads to apoptotic volume decrease (AVD) of the cell. Both mitochondrion-mediated intrinsic, and death receptor-mediated extrinsic, apoptotic stimuli have been reported to rapidly activate Cl(-) conductances in a large variety of cell types. In epithelial cells and cardiomyocytes, the AVD-inducing anion channel was recently determined to be the volume-sensitive outwardly rectifying (VSOR) Cl(-) channel which is usually activated by swelling under non-apoptotic conditions. Blocking the VSOR Cl(-) channel prevented cell death in not only epithelial and cardiac cells, but also other cell types, by inhibiting the induction of AVD and subsequent apoptotic events. Ischemia-reperfusion-induced apoptotic death in cardiomyocytes and brain neurons was also prevented by Cl(-) channel blockers. Furthermore, cancer cell apoptosis induced by the anti-cancer drug cisplatin was recently found to be associated with augmented activity of the VSOR Cl(-) channel and to be inhibited by a Cl(-) channel blocker. The apoptosis-inducing VSOR Cl(-) channel is distinct from ClC-3 and its molecular identity remains to be determined.

Indexed as

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic AcidAnimalsApoptosisCell DeathCell SizeChloride ChannelsHumansMyocytes, CardiacStaurosporine4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic AcidChloride ChannelsStaurosporine

Identifiers

PMID16685598
OpenAlexW2055981402

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.