Evidence map›Paper›PMID 22555917›Full record

ReviewPflugers Archiv : European journal of physiology2012

Mitochondrial regulation of cytosolic Ca²⁺ signals in smooth muscle.

John G McCarron, Marnie L Olson, Susan Chalmers

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pflugers Archiv : European journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. CaPhysiological reviews · 2024
    Review
  2. Article
  3. Article
  4. Article
  5. CaMKII (CaArteriosclerosis, thrombosis, and vascular biology · 2018
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Nitric oxide regulates vascular adaptive mitochondrial dynamics.American journal of physiology. Heart and circulatory physiology · 2013
    Article
  14. Calcium dynamics in vascular smooth muscle.Microcirculation (New York, N.Y. : 1994) · 2013
    Review
  15. Review
  16. A Special Issue on the cell-specific roles of mitochondrial Ca²⁺ handling.Pflugers Archiv : European journal of physiology · 2012
    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

3 authors at 1 institution in 1 country.

John G McCarronStrathclyde Institute of Pharmacy & Biomedical Sciences, University of Strathclyde, John Arbuthnott Building, 161 Cathedral Street, Glasgow, G4 0NR, UK. john.mccarron@strath.ac.uk
Marnie L Olson
Susan Chalmers
University of Strathclyde · GB

Funding

British Heart Foundation PG/11/70/29086Wellcome Trust 092292/Z/10/Z
6 · The paper itself

Abstract

The cytosolic Ca²⁺ concentration ([Ca²⁺]c) controls virtually every activity of smooth muscle, including contraction, migration, transcription, division and apoptosis. These processes may be activated by large (>10 μM) amplitude [Ca²⁺]c increases, which occur in small restricted regions of the cell or by smaller (<1 μM) amplitude changes throughout the bulk cytoplasm. Mitochondria contribute to the regulation of these signals by taking up Ca²⁺. However, mitochondria's reported low affinity for Ca²⁺ is thought to require the organelle to be positioned close to ion channels and within a microdomain of high [Ca²⁺]. In cultured smooth muscle, mitochondria are highly dynamic structures but in native smooth muscle mitochondria are immobile, apparently strategically positioned organelles that regulate the upstroke and amplitude of IP₃-evoked Ca²⁺ signals and IP₃ receptor (IP₃R) cluster activity. These observations suggest mitochondria are positioned within the high [Ca²⁺] microdomain arising from an IP₃R cluster to exert significant local control of channel activity. On the other hand, neither the upstroke nor amplitude of voltage-dependent Ca²⁺ entry is modulated by mitochondria; rather, it is the declining phase of the transient that is regulated by the organelle. Control of the declining phase of the transient requires a high mitochondrial affinity for Ca²⁺ to enable uptake to occur over the normal physiological Ca²⁺ range (<1 μM). Thus, in smooth muscle, mitochondria regulate Ca²⁺ signals exerting effects over a large range of [Ca²⁺] (∼200 nM to at least tens of micromolar) to provide a wide dynamic range in the control of Ca²⁺ signals.

Indexed as

Calcium SignalingAnimalsCalciumCalcium ChannelsCytosolHumansMembrane Potential, MitochondrialMitochondriaMyocytes, Smooth MuscleCalciumCalcium Channels

Identifiers

PMID22555917
OpenAlexW2127710212

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.