Evidence map›Paper›PMID 11768760›Full record

ReviewJournal of bioenergetics and biomembranes2000

Mitochondria in Ca2+ signaling and apoptosis.

S S Smaili, Y T Hsu, R J Youle, J T Russell

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of bioenergetics and biomembranes, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

41 citing papers in PubMed, 164 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Metal ions overloading and cell death.Cell biology and toxicology · 2024
    Review
  7. Review
  8. NAADP-Evoked CaInternational journal of molecular sciences · 2023
    Article
  9. HybridACS pharmacology & translational science · 2021
    Article
  10. Ultrastructure of Cells and Microanalysis inMolecules (Basel, Switzerland) · 2020
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
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 3 institutions in 2 countries.

S S SmailiLaboratory of Cellular and Molecular Neurophysiology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892-4495, USA.
Y T Hsu
R J Youle
J T Russell
National Institutes of Health · USNational Institute of Neurological Disorders and Stroke · USUniversidade Federal de São Paulo · BR

Funding

RECEPTOR MEDIATED CALCIUM SIGNALLING IN GLIA NEURONSZ01HD001206 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI RUSSELL, JAMES T. · 1994 to 2008
$1.0M
Receptor Mediated Calcium Signaling In Glia And NeuronsZIAHD001206 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI RUSSELL, JAMES T. · 2009 to 2011
$152k
6 · The paper itself

Abstract

Cellular Ca2+ signals are crucial in the control of most physiological processes, cell injury and programmed cell death; mitochondria play a pivotal role in the regulation of such cytosolic Ca2+ ([Ca2+]c) signals. Mitochondria are endowed with multiple Ca2+ transport mechanisms by which they take up and release Ca2+ across their inner membrane. These transport processes function to regulate local and global [Ca2+]c, thereby regulating a number of Ca2+-sensitive cellular mechanisms. The permeability transition pore (PTP) forms the major Ca2+ efflux pathway from mitochondria. In addition, Ca2+ efflux from the mitochondrial matrix occurs by the reversal of the uniporter and through the inner membrane Na+/Ca2+ exchanger. During cellular Ca2+ overload, mitochondria take up [Ca2+]c, which, in turn, induces opening of PTP, disruption of mitochondrial membrane potential (delta(psi)m) and cell death. In apoptosis signaling, collapse of delta(psi)m and cytochrome c release from mitochondria occur followed by activation of caspases, DNA fragmentation, and cell death. Translocation of Bax, an apoptotic signaling protein from the cytosol to the mitochondrial membrane, is another step during this apoptosis-signaling pathway. The role of permeability transition in the context of cell death in relation to Bcl-2 family of proteins is discussed.

Indexed as

ApoptosisCalcium SignalingAnimalsCell DeathIntracellular MembranesMitochondriaPermeabilityProto-Oncogene Proteins c-bcl-2Proto-Oncogene Proteins c-bcl-2

Identifiers

PMID11768760
OpenAlexW153349786

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.