Evidence map›Paper›PMID 32613144›Full record

ArticleJACC. Basic to translational science2020

In Mice Subjected to Chronic Stress, Exogenous cBIN1 Preserves Calcium-Handling Machinery and Cardiac Function.

Yan Liu, Kang Zhou, Jing Li, Sosse Agvanian, Ana-Maria Caldaruse, Seiji Shaw, Tara C Hitzeman, Robin M Shaw, TingTing Hong

Abstract read
In one paragraph

Article in JACC. Basic to translational science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
–field-weighted citation impact
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

25 citing papers in PubMed.

  1. Review
  2. Past, Present and Future of Regenerative Gene Therapy for Ischemic Heart Failure.Journal of cardiovascular translational research · 2026
    Review
  3. Article
  4. BIN1 gene replacement reverses BIN1-related centronuclear myopathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  5. TREK-1: a Janus-faced and subcellular location-based regulator of cardiac remodeling in heart failure.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  6. Bend it like BIN1: how a membrane-curving adaptor protein shapes cardiac physiology.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Enhanced CaJACC. Clinical electrophysiology · 2024
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Huntington's disease skeletal muscle has altered T-tubules.The Journal of general physiology · 2021
    Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Yan LiuSmidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Kang ZhouSmidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Jing LiSmidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Sosse AgvanianSmidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Ana-Maria CaldaruseSmidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Seiji ShawSmidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Tara C HitzemanNora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, Utah.
Robin M ShawNora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, Utah.
TingTing HongSmidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California.

Funding

Regulation of Ion Channels at BIN1-induced T-tubule MicrodomainsR01HL133286 · NHLBI · UNIVERSITY OF UTAH · PI HONG, TINGTING · 2016 to 2020
$2.2M
A New Non-Canonical Role for an Alternatively Translated Ion Channel ProteinR01HL138577 · NHLBI · UNIVERSITY OF UTAH · PI SHAW, ROBIN M · 2017 to 2020
$2.1M
Unlocking Trafficking Specificity for Cx43 Gap JunctionsR01HL152691 · NHLBI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Robin M Shaw · 2020 to 2026
$2.0M
NHLBI NIH HHS R01 HL133286NHLBI NIH HHS R01 HL138577NHLBI NIH HHS R01 HL152691
6 · The paper itself

Abstract

Heart failure is an important, and growing, cause of morbidity and mortality. Half of patients with heart failure have preserved ejection fraction, for whom therapeutic options are limited. Here we report that cardiac bridging integrator 1 gene therapy to maintain subcellular membrane compartments within cardiomyocytes can stabilize intracellular distribution of calcium-handling machinery, preserving diastolic function in hearts stressed by chronic beta agonist stimulation and pressure overload. This study identifies that maintenance of intracellular architecture and, in particular, membrane microdomains at t-tubules, is important in the setting of sympathetic stress. Stabilization of membrane microdomains may be a pathway for future therapeutic development.

Indexed as

AAV9, adeno-associated virus 9ANOVA, analysis of varianceAR, adrenergic receptorATPase, adenosine triphosphataseBW, body weightCAMKII, Ca2+/calmodulin-dependent protein kinasecBIN1, cardiac bridging integrator 1CMV, cytomegalovirusDi-8-ANNEPs, 4-[2-[6-(Dioctylamino)-2-naphthalenyl]ethenyl]-1-(3-sulfopropyl)-pyridinium, inner saltdiastolic dysfunctionEC, excitation contractionEDV, end diastolic volumeEF, ejection fractionGFP, green fluorescent proteinheart failureHF, heart failureHR, heart rateHT, heterozygoteHW, heart weightISO, isoproterenoljSR, junctional sarcoplasmic reticulumLSD, least significant differenceLTCC, voltage-dependent L-type calcium channelLV, left ventricularLW, lung weightPBS, phosphate-buffered salinePKA, protein kinase APLN, phospholambanpressure overloadRWT, relative wall thicknessRyR, ryanodine receptorSD, standard deviationSEM, standard error of the meanSERCA2a, sarcoplasmic reticulum calcium ATPase pump 2aSR, sarcoplasmic reticulumSTORM, stochastic optical reconstruction microscopysympathetic overdriveTAC, transverse aortic constrictionTEM, transmission electron microscopyt-tubulet-tubule, transverse-tubulevg, vector genomeWT, wild type

Identifiers

PMID32613144
PMCPMC7315191

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.