Evidence map›Paper›PMID 33669042›Full record

ReviewInternational journal of molecular sciences2021

Cardiac T-Tubule cBIN1-Microdomain, a Diagnostic Marker and Therapeutic Target of Heart Failure.

Jing Li, Bradley Richmond, TingTing Hong

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. Cardiac Cell Remodeling in Obesity and Diabetes.Handbook of experimental pharmacology · 2026
    Review
  4. BIN1 gene replacement reverses BIN1-related centronuclear myopathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  5. Bend it like BIN1: how a membrane-curving adaptor protein shapes cardiac physiology.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  6. Article
  7. BIN1 reduction amelioratesProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. [Association between serum BIN1 level and Killip class in patients with acute myocardial infraction].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024
    Article
  9. Review
  10. Article
  11. Emerging New Biomarkers for Cardiovascular Disease.International journal of molecular sciences · 2022
    Article
  12. Review
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.

Jing LiDepartment of Pharmacology and Toxicology, College of Pharmacy, University of Utah, Salt Lake City, UT 84112, USA.ORCID 0000-0003-4613-260X
Bradley RichmondDepartment of Pharmacology and Toxicology, College of Pharmacy, University of Utah, Salt Lake City, UT 84112, USA.
TingTing HongDepartment of Pharmacology and Toxicology, College of Pharmacy, University of Utah, Salt Lake City, UT 84112, USA.ORCID 0000-0002-0243-5046
University of Utah · US

Funding

NIH HHS HL133286
6 · The paper itself

Abstract

Since its first identification as a cardiac transverse tubule (t-tubule) protein, followed by the cloning of the cardiac isoform responsible for t-tubule membrane microdomain formation, cardiac bridging integrator 1 (cBIN1) and its organized microdomains have emerged as a key mechanism in maintaining normal beat-to-beat heart contraction and relaxation. The abnormal remodeling of cBIN1-microdomains occurs in stressed and diseased cardiomyocytes, contributing to the pathophysiology of heart failure. Due to the homeostatic turnover of t-tubule cBIN1-microdomains via microvesicle release into the peripheral circulation, plasma cBIN1 can be assayed as a liquid biopsy of cardiomyocyte health. A new blood test cBIN1 score (CS) has been developed as a dimensionless inverse index derived from plasma cBIN1 concentration with a diagnostic and prognostic power for clinical outcomes in stable ambulatory patients with heart failure with reduced or preserved ejection fraction (HFrEF or HFpEF). Recent evidence further indicates that exogenous cBIN1 introduced by adeno-associated virus 9-based gene therapy can rescue cardiac contraction and relaxation in failing hearts. The therapeutic potential of cBIN1 gene therapy is enormous given its ability to rescue cardiac inotropy and provide lusitropic protection in the meantime. These unprecedented capabilities of cBIN1 gene therapy are shifting the current paradigm of therapy development for heart failure, particularly HFpEF.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsBiomarkersCalcium SignalingGenetic TherapyHeart FailureHumansMembrane ProteinsMyocardial ContractionMyocytes, CardiacNuclear ProteinsProtein DomainsSarcolemmaSarcoplasmic ReticulumTumor Suppressor ProteinsAdaptor Proteins, Signal TransducingBIN1 protein, humanBiomarkersMembrane ProteinsNuclear ProteinsTumor Suppressor Proteinsbiomarkercalcium handlingcBIN1gene therapyheart failureT-tubules

Identifiers

PMID33669042
PMCPMC7956774
OpenAlexW3131002254

What Socratic 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 Socratic graph.