Evidence map›Paper›PMID 27150728›Full record

ArticleScientific reports2016

STIM1-dependent Ca(2+) microdomains are required for myofilament remodeling and signaling in the heart.

Cory Parks, Mohammad Afaque Alam, Ryan Sullivan, Salvatore Mancarella

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Analysis ofAmerican journal of physiology. Heart and circulatory physiology · 2022
    Article
  8. Review
  9. Article
  10. The interplay between mitochondria and store-operated CaJournal of cellular and molecular medicine · 2021
    Review
  11. Review
  12. Article
  13. SOCE in the cardiomyocyte: the secret is in the chambers.Pflugers Archiv : European journal of physiology · 2021
    Review
  14. TRIC-A regulates intracellular CaPflugers Archiv : European journal of physiology · 2021
    Review
  15. Store-Operated Calcium Entry in the Cardiovascular System.Advances in experimental medicine and biology · 2021
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  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 1 institution in 1 country.

Cory ParksDepartment of Physiology Medicine, University of Tennessee Health Sciences Center, Memphis, TN 38163, USA.
Mohammad Afaque AlamDepartment of Physiology Medicine, University of Tennessee Health Sciences Center, Memphis, TN 38163, USA.
Ryan SullivanDepartment of Comparative Medicine, University of Tennessee Health Sciences Center, Memphis, TN 38163, USA.
Salvatore MancarellaDepartment of Physiology Medicine, University of Tennessee Health Sciences Center, Memphis, TN 38163, USA.
University of Tennessee Health Science Center · US

Funding

STIM-Dependent Signaling in Cardiac PathophysiologyR00HL114869 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI MANCARELLA, SALVATORE · 2016 to 2018
$738k
STIM-Dependent Signaling in Cardiac PathophysiologyK99HL114869 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI MANCARELLA, SALVATORE · 2013 to 2014
$208k
NHLBI NIH HHS K99 HL114869NHLBI NIH HHS R00 HL114869
6 · The paper itself

Abstract

In non-excitable cells stromal interaction molecule 1 (STIM1) is a key element in the generation of Ca(2+) signals that lead to gene expression, migration and cell proliferation. A growing body of literature suggests that STIM1 plays a key role in the development of pathological cardiac hypertrophy. However, the precise mechanisms involving STIM-dependent Ca(2+) signaling in the heart are not clearly established. Here, we have investigated the STIM1-associated Ca(2+) signals in cardiomyocytes and their relevance to pathological cardiac remodeling. We show that mice with inducible, cardiac-restricted, ablation of STIM1 exhibited left ventricular reduced contractility, which was corroborated by impaired single cell contractility. The spatial properties of STIM1-dependent Ca(2+) signals determine restricted Ca(2+) microdomains that regulate myofilament remodeling and activate spatially segregated pro-hypertrophic factors. Indeed, mice lacking STIM1 showed less adverse structural remodeling in response to pressure overload-induced cardiac hypertrophy. These results highlight how STIM1-dependent Ca(2+) microdomains have a major impact on intracellular Ca(2+) homeostasis, cytoskeletal remodeling and cellular signaling, even when excitation-contraction coupling is present.

Indexed as

Calcium SignalingAnimalsCells, CulturedGene Knockdown TechniquesHeartMembrane MicrodomainsMiceMyocardial ContractionMyocytes, CardiacMyofibrilsRatsStromal Interaction Molecule 1Stim1 protein, mouseStromal Interaction Molecule 1

Identifiers

PMID27150728
PMCPMC4858716
OpenAlexW2345533718

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.