Evidence map›Paper›PMID 33511120›Full record

ReviewFrontiers in cell and developmental biology2020

Cell Death Induction and Protection by Activation of Ubiquitously Expressed Anion/Cation Channels. Part 1: Roles of VSOR/VRAC in Cell Volume Regulation, Release of Double-Edged Signals and Apoptotic/Necrotic Cell Death.

Yasunobu Okada, Ravshan Z Sabirov, Kaori Sato-Numata, Tomohiro Numata

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 39 citations in OpenAlex.

  1. Chronic hyponatremia and skeletal vulnerability: bone loss, fragility fracture risk, and therapeutic uncertainties.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. The function of chloride channels in digestive system disease (Review).International journal of molecular medicine · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Piezo1, the new actor in cell volume regulation.Pflugers Archiv : European journal of physiology · 2024
    Review
  11. Review
  12. Review
  13. Mechanosensing in Metabolism.Comprehensive Physiology · 2023
    Review
  14. Review
  15. Article
  16. Review
  17. Apoptotic volume decrease (AVD) in AFrontiers in physiology · 2023
    Article
  18. Modulation ofJournal of pharmacopuncture · 2022
    Article
  19. Review
  20. Review
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 4 institutions in 2 countries.

Yasunobu OkadaNational Institute for Physiological Sciences, Okazaki, Japan.
Ravshan Z SabirovLaboratory of Molecular Physiology, Institute of Biophysics and Biochemistry, National University of Uzbekistan, Tashkent, Uzbekistan.
Kaori Sato-NumataJapan Society for the Promotion of Science, Tokyo, Japan.
Tomohiro NumataDepartment of Physiology, School of Medicine, Fukuoka University, Fukuoka, Japan.
Aichi Medical University · JPFukuoka University · JPJapan Society for the Promotion of Science · JPNational University of Uzbekistan · UZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell volume regulation (CVR) is essential for survival and functions of animal cells. Actually, normotonic cell shrinkage and swelling are coupled to apoptotic and necrotic cell death and thus called the apoptotic volume decrease (AVD) and the necrotic volume increase (NVI), respectively. A number of ubiquitously expressed anion and cation channels are involved not only in CVD but also in cell death induction. This series of review articles address the question how cell death is induced or protected with using ubiquitously expressed ion channels such as swelling-activated anion channels, acid-activated anion channels and several types of TRP cation channels including TRPM2 and TRPM7. The Part 1 focuses on the roles of the volume-sensitive outwardly rectifying anion channels (VSOR), also called the volume-regulated anion channel (VRAC), which is activated by cell swelling or reactive oxygen species (ROS) in a manner dependent on intracellular ATP. First we describe phenotypical properties, the molecular identity, and physical pore dimensions of VSOR/VRAC. Second, we highlight the roles of VSOR/VRAC in the release of organic signaling molecules, such as glutamate, glutathione, ATP and cGAMP, that play roles as double-edged swords in cell survival. Third, we discuss how VSOR/VRAC is involved in CVR and cell volume dysregulation as well as in the induction of or protection from apoptosis, necrosis and regulated necrosis under pathophysiological conditions.

Indexed as

apoptotic cell deathcell volume regulationcisplatin resistanceglutamate releaseGSH releasenecrotic cell deathprogrammed necrosisVSOR/VRAC

Identifiers

PMID33511120
PMCPMC7835517
OpenAlexW3118735898

What OpenQuestion holds

Textmetadata
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.