Evidence map›Paper›PMID 14754504›Full record

ReviewJournal of cellular and molecular medicine

Endoplasmic reticulum Ca(2+) homeostasis and neuronal death.

A Verkhratsky, E C Toescu

Abstract readReview
In one paragraph

Review in Journal of cellular and molecular medicine. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
–field-weighted citation impact
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

53 citing papers in PubMed.

  1. Review
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  8. The NaFrontiers in pharmacology · 2021
    Article
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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.

A VerkhratskyThe University of Manchester, School of Biological Sciences, Manchester, United Kingdom. alex.verkhratsky@man.ac.uk
E C Toescu

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The endoplasmic reticulum (ER) is a universal signalling organelle, which regulates a wide range of neuronal functional responses. Calcium release from the ER underlies various forms of intracellular Ca(2+) signalling by either amplifying Ca(2+) entry through voltage-gated Ca(2+) channels by Ca(2+)-induced Ca(2+) release (CICR) or by producing local or global cytosolic calcium fluctuations following stimulation of metabotropic receptors through inositol-1,4,5-trisphosphate-induced Ca(2+) release (IICR). The ER Ca(2+) store emerges as a single interconnected pool, thus allowing for a long-range Ca(2+) signalling via intra-ER tunnels. The fluctuations of intra-ER free Ca(2+) concentration regulate the activity of numerous ER resident proteins responsible for post-translational protein folding and modification. Disruption of ER Ca(2+) homeostasis results in the developing of ER stress response, which in turn controls neuronal survival. Altered ER Ca(2+) handling may be involved in pathogenesis of various neurodegenerative diseases including brain ischemia and Alzheimer dementia.

Indexed as

Calcium SignalingAlzheimer DiseaseAnimalsApoptosisBrain IschemiaCalcium ChannelsEndoplasmic ReticulumHomeostasisHumansModels, NeurologicalNeuronsCalcium Channels

Identifiers

PMID14754504
PMCPMC6740085

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.