Evidence map›Paper›PMID 10793156›Full record

ArticleMolecular biology of the cell2000

Inositol 1,4,5-trisphosphate directs Ca(2+) flow between mitochondria and the Endoplasmic/Sarcoplasmic reticulum: a role in regulating cardiac autonomic Ca(2+) spiking.

M Jaconi, C Bony, S M Richards, A Terzic, S Arnaudeau, G Vassort, M Pucéat

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.4field-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

25 citing papers in PubMed, 98 citations in OpenAlex.

  1. Mitochondrial dysfunction and CaScientific reports · 2026
    Article
  2. Article
  3. Review
  4. Article
  5. An integrated mechanism of cardiomyocyte nuclear Ca(2+) signaling.Journal of molecular and cellular cardiology · 2014
    Review
  6. Article
  7. Article
  8. Developmental aspects of cardiac Ca(2+) signaling: interplay between RyR- and IP(3)R-gated Ca(2+) stores.American journal of physiology. Heart and circulatory physiology · 2010
    Article
  9. Review
  10. Review
  11. Emerging roles of inositol 1,4,5-trisphosphate signaling in cardiac myocytes.Journal of molecular and cellular cardiology · 2008
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Calreticulin in the heart.Molecular and cellular biochemistry · 2004
    Article
  19. Article
  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

7 authors at 4 institutions in 3 countries.

M JaconiInstitut National de la Santé et de la Recherche Médicale U-390, CHU Arnaud de Villeneuve, Montpellier, 34295 France.
C Bony
S M Richards
A Terzic
S Arnaudeau
G Vassort
M Pucéat
Inserm · FRCentre National de la Recherche Scientifique · FRHôpital Beau-Séjour · CHMayo Clinic · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The signaling role of the Ca(2+) releaser inositol 1,4, 5-trisphosphate (IP(3)) has been associated with diverse cell functions. Yet, the physiological significance of IP(3) in tissues that feature a ryanodine-sensitive sarcoplasmic reticulum has remained elusive. IP(3) generated by photolysis of caged IP(3) or by purinergic activation of phospholipase Cgamma slowed down or abolished autonomic Ca(2+) spiking in neonatal rat cardiomyocytes. Microinjection of heparin, blocking dominant-negative fusion protein, or anti-phospholipase Cgamma antibody prevented the IP(3)-mediated purinergic effect. IP(3) triggered a ryanodine- and caffeine-insensitive Ca(2+) release restricted to the perinuclear region. In cells loaded with Rhod2 or expressing a mitochondria-targeted cameleon and TMRM to monitor mitochondrial Ca(2+) and potential, IP(3) induced transient Ca(2+) loading and depolarization of the organelles. These mitochondrial changes were associated with Ca(2+) depletion of the sarcoplasmic reticulum and preceded the arrest of cellular Ca(2+) spiking. Thus, IP(3) acting within a restricted cellular region regulates the dynamic of calcium flow between mitochondria and the endoplasmic/sarcoplasmic reticulum. We have thus uncovered a novel role for IP(3) in excitable cells, the regulation of cardiac autonomic activity.

Indexed as

Adenosine TriphosphateAmino Acid SequenceAnimalsAntibodiesCaffeineCalciumCalcium ChannelsCalcium SignalingCells, CulturedEndoplasmic ReticulumFluorescent DyesHeartHeparinInositol 1,4,5-TrisphosphateInositol 1,4,5-Trisphosphate ReceptorsIsoenzymesAdenosine TriphosphateAntibodiesCaffeineCalciumCalcium ChannelsFluorescent DyesHeparinInositol 1,4,5-TrisphosphateInositol 1,4,5-Trisphosphate ReceptorsIsoenzymesPhospholipase C gammaReceptors, Cytoplasmic and NuclearRecombinant Fusion ProteinsRyanodineType C Phospholipases

Identifiers

PMID10793156
PMCPMC14888
OpenAlexW2110471341

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.