Evidence map›Paper›PMID 15545319›Full record

ArticleThe Journal of cell biology2004

Control of mitochondrial motility and distribution by the calcium signal: a homeostatic circuit.

Muqing Yi, David Weaver, György Hajnóczky

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 242 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
242citing papers in PubMed, 1 pooled it
8.4field-weighted citation impact, top 1% 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

242 citing papers in PubMed, 1 synthesis or guideline pooled it, 481 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Mitochondrial Calcium Signaling in Hepatocyte Health and Disease.Cold Spring Harbor perspectives in biology · 2026
    Review
  4. Article
  5. Article
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  7. The intermediate filament protein GFAP regulates mitochondrial fission in astrocytes.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Molecular mechanisms of mitochondrial quality control.Translational neurodegeneration · 2025
    Review
  9. Review
  10. Article
  11. The genetic landscape of pediatric postural orthostatic tachycardia syndrome.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2025
    Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

182 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

3 authors at 1 institution in 1 country.

Muqing YiDepartment of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA 19107, USA.
David Weaver
György Hajnóczky
Thomas Jefferson University · US

Funding

Mechanisms of Pulsatile Calcium SignalingR01DK051526 · NIDDK · THOMAS JEFFERSON UNIVERSITY · PI HAJNOCZKY, GYORGY · 2001 to 2016
$4.3M
NIDDK NIH HHS R01 DK051526NIDDK NIH HHS R01 DK51526
6 · The paper itself

Abstract

Mitochondria are dynamic organelles in cells. The control of mitochondrial motility by signaling mechanisms and the significance of rapid changes in motility remains elusive. In cardiac myoblasts, mitochondria were observed close to the microtubular array and displayed both short- and long-range movements along microtubules. By clamping cytoplasmic [Ca2+] ([Ca2+]c) at various levels, mitochondrial motility was found to be regulated by Ca2+ in the physiological range. Maximal movement was obtained at resting [Ca2+]c with complete arrest at 1-2 microM. Movement was fully recovered by returning to resting [Ca2+]c, and inhibition could be repeated with no apparent desensitization. The inositol 1,4,5-trisphosphate- or ryanodine receptor-mediated [Ca2+]c signal also induced a decrease in mitochondrial motility. This decrease followed the spatial and temporal pattern of the [Ca2+]c signal. Diminished mitochondrial motility in the region of the [Ca2+]c rise promotes recruitment of mitochondria to enhance local Ca2+ buffering and energy supply. This mechanism may provide a novel homeostatic circuit in calcium signaling.

Indexed as

HomeostasisActin CytoskeletonCalciumCalcium SignalingCell LineCytoplasmic StreamingHumansIntracellular MembranesMembrane PotentialsMicrotubulesMitochondriaMyoblasts, CardiacRyanodine Receptor Calcium Release ChannelCalciumRyanodine Receptor Calcium Release Channel

Identifiers

PMID15545319
PMCPMC2172592
OpenAlexW2165601218

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.