Evidence map›Paper›PMID 36647824›Full record

ReviewThe Journal of clinical investigation2023

Targeting ryanodine receptors to treat human diseases.

Andrew R Marks

Open access · goldAbstract readReview
In one paragraph

Review in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
10.8field-weighted citation impact, top 1% 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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. An RYR2-interacting fragment of MYBPC3 mitigates arrhythmia in human iPSC-CM and mouse models of CPVT.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
  5. VMP1 forms a CaScience advances · 2026
    Article
  6. eLife · 2026
    Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Synergistic antiarrhythmic mechanism of IJournal of translational medicine · 2025
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  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

1 author at 1 institution in 1 country.

Andrew R Marks
Columbia University · US

Funding

Exploring the Molecular Physiology of Atrial FibrillationR01HL140934 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI MARKS, ANDREW ROBERT, MARX, STEVEN O · 2018 to 2025
$6.0M
Training in Cardiovascular Translational ResearchT32HL120826 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI MARKS, ANDREW ROBERT, TABAS, IRA A · 2014 to 2023
$4.7M
Structure-function analysis for elucidating pathogenicity of cardiac ryanodine receptor genetic variantsR01HL145473 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI MARKS, ANDREW ROBERT, SHEPARD, KENNETH L · 2019 to 2022
$3.1M
LIVOPT -- LIVer cirrhosis - Optimizing Prediction of Patient OuTcomesR01AG070194 · NIA · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LADNER, DANIELA P, MEHROTRA, SANJAY · 2021 to 2025
$3.1M
Ryanodine Receptor Defects in Cardiomyopathy Caused by Lamin A/C Gene MutationsR01HL142903 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI MARKS, ANDREW ROBERT, WORMAN, HOWARD J · 2019 to 2022
$1.8M
Calcium and the physiology of diabetesR01DK118240 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI MARKS, ANDREW ROBERT · 2019 to 2022
$1.6M
Summer Program for Under Represented Students (SPURS)R25NS076445 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Wesley B Grueber, STEVEN A SIEGELBAUM · 2012 to 2026
$1.4M
Training in Cardiovascular Sciences for Under Represented StudentsR25HL156002 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI MARKS, ANDREW ROBERT · 2021 to 2025
$624k
NHLBI NIH HHS R01 HL140934NHLBI NIH HHS R01 HL142903NHLBI NIH HHS R01 HL145473NHLBI NIH HHS R25 HL156002NHLBI NIH HHS T32 HL120826NIA NIH HHS R01 AG070194NIDDK NIH HHS R01 DK118240NINDS NIH HHS R25 NS076445
6 · The paper itself

Abstract

This Review provides an update on ryanodine receptors (RyRs) and their role in human diseases of heart, muscle, and brain. Calcium (Ca2+) is a requisite second messenger in all living organisms. From C. elegans to mammals, Ca2+ is necessary for locomotion, bodily functions, and neural activity. However, too much of a good thing can be bad. Intracellular Ca2+ overload can result in loss of function and death. Intracellular Ca2+ release channels evolved to safely provide large, rapid Ca2+ signals without exposure to toxic extracellular Ca2+. RyRs are intracellular Ca2+ release channels present throughout the zoosphere. Over the past 35 years, our knowledge of RyRs has advanced to the level of atomic-resolution structures revealing their role in the mechanisms underlying the pathogenesis of human disorders of heart, muscle, and brain. Stress-induced RyR-mediated intracellular Ca2+ leak in the heart can promote heart failure and cardiac arrhythmias. In skeletal muscle, RyR1 leak contributes to muscle weakness in inherited myopathies, to age-related loss of muscle function and cancer-associated muscle weakness, and to impaired muscle function in muscular dystrophies, including Duchenne. In the brain, leaky RyR channels contribute to cognitive dysfunction in Alzheimer's disease, posttraumatic stress disorder, and Huntington's disease. Novel therapeutics targeting dysfunctional RyRs are showing promise.

Indexed as

CalciumRyanodine Receptor Calcium Release ChannelHumansMuscle, SkeletalMuscle WeaknessCalciumRyanodine Receptor Calcium Release Channel

Identifiers

PMID36647824
PMCPMC9843046
OpenAlexW4316661363

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.