Evidence map›Paper›PMID 36724092›Full record

ArticleeLife2023

Muscle calcium stress cleaves junctophilin1, unleashing a gene regulatory program predicted to correct glucose dysregulation.

Eshwar R Tammineni, Lourdes Figueroa, Carlo Manno, Disha Varma, Natalia Kraeva, Carlos A Ibarra, Amira Klip, Sheila Riazi, Eduardo Rios

Open access · goldAbstract read
In one paragraph

Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

11 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Skeletal muscle disorders as risk factors for type 2 diabetes.Molecular and cellular endocrinology · 2025
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  6. Article
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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

9 authors at 3 institutions in 2 countries.

Eshwar R TammineniDepartment of Physiology and Biophysics, Rush University, Chicago, United States.ORCID 0000-0001-7290-9326
Lourdes FigueroaDepartment of Physiology and Biophysics, Rush University, Chicago, United States.
Carlo MannoDepartment of Physiology and Biophysics, Rush University, Chicago, United States.
Disha VarmaDepartment of Internal Medicine, Division of Nephrology, Rush University, Chicago, United States.
Natalia KraevaDepartment of Anesthesia & Pain Management, University of Toronto, Toronto, Canada.
Carlos A IbarraDepartment of Anesthesia & Pain Management, University of Toronto, Toronto, Canada.ORCID 0000-0001-8898-6772
Amira KlipCell Biology Program, The Hospital for Sick Children, Toronto, Canada.ORCID 0000-0001-7906-0302
Sheila RiaziDepartment of Anesthesia & Pain Management, University of Toronto, Toronto, Canada.
Eduardo RiosDepartment of Physiology and Biophysics, Rush University, Chicago, United States.ORCID 0000-0003-0985-8997
Rush University · USUniversity of Toronto · CAHospital for Sick Children · CA

Funding

Mechanisms of couplon-linked skeletal muscle myopathiesR01AR072602 · NIAMS · BAYLOR COLLEGE OF MEDICINE · PI HAMILTON, SUSAN L, HORRIGAN, FRANK T · 2018 to 2022
$3.3M
The HH: A Large Cohort of Patients with Congenital Myopathies of Uncertain EtiologyR01AR071381 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI FILL, MICHAEL, RIAZI, SHEILA · 2017 to 2021
$2.7M
Roles of Calsequestrin in the Control of Calcium Signals in Health and DiseaseR01GM111254 · NIGMS · RUSH UNIVERSITY MEDICAL CENTER · PI KANG, CHULHEE, RIOS, EDUARDO · 2014 to 2017
$1.4M
Dual Confocal Microscopic ScannerS10RR024707 · NCRR · RUSH UNIVERSITY MEDICAL CENTER · PI RIOS, EDUARDO · 2008 to 2008
$500k
NCRR NIH HHS S1055024707NCRR NIH HHS S10 RR024707NIAMS NIH HHS R01 AR071381NIAMS NIH HHS R01AR071381NIAMS NIH HHS R01 AR072602NIAMS NIH HHS R01AR072602NIGMS NIH HHS R01 GM111254NIGMS NIH HHS R01GM111254
6 · The paper itself

Abstract

Calcium ion movements between cellular stores and the cytosol govern muscle contraction, the most energy-consuming function in mammals, which confers skeletal myofibers a pivotal role in glycemia regulation. Chronic myoplasmic calcium elevation ("calcium stress"), found in malignant hyperthermia-susceptible (MHS) patients and multiple myopathies, has been suggested to underlie the progression from hyperglycemia to insulin resistance. What drives such progression remains elusive. We find that muscle cells derived from MHS patients have increased content of an activated fragment of GSK3β - a specialized kinase that inhibits glycogen synthase, impairing glucose utilization and delineating a path to hyperglycemia. We also find decreased content of junctophilin1, an essential structural protein that colocalizes in the couplon with the voltage-sensing Ca

Indexed as

HyperglycemiaMalignant HyperthermiaAnimalsCalciumCalcium, DietaryDisease SusceptibilityGlucoseGlycogen Synthase Kinase 3 betaHumansMammalsMembrane ProteinsMuscle, SkeletalRyanodine Receptor Calcium Release ChannelCalciumCalcium, DietaryGlucoseGlycogen Synthase Kinase 3 betajunctophilinMembrane ProteinsRyanodine Receptor Calcium Release Channelglucose transporthumanimmunocytochemistrymolecular biophysicsmousephosphorylationprotein kinasestructural biologytranscription factors

Identifiers

PMID36724092
PMCPMC9891728
OpenAlexW4318753917

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.