Evidence map›Paper›PMID 33430602›Full record

ArticleCirculation. Heart failure2021

Proteomic and Functional Studies Reveal Detyrosinated Tubulin as Treatment Target in Sarcomere Mutation-Induced Hypertrophic Cardiomyopathy.

Maike Schuldt, Jiayi Pei, Magdalena Harakalova, Larissa M Dorsch, Saskia Schlossarek, Michal Mokry, Jaco C Knol, Thang V Pham, Tim Schelfhorst, Sander R Piersma and 9 more

Open access · hybridAbstract read
In one paragraph

Article in Circulation. Heart failure, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
11.8field-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

70 citing papers in PubMed, 98 citations in OpenAlex.

  1. Observational
  2. Article
  3. Why the septum thickens in hypertrophic cardiomyopathy.Journal of molecular and cellular cardiology plus · 2026
    Review
  4. Article
  5. iScience · 2026
    Article
  6. Peptide-based covalent inhibitor of tubulin detyrosination promotes mesenchymal-to-epithelial transition in lung cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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10 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 7 institutions in 5 countries.

Maike SchuldtAmsterdam UMC, Vrije Universiteit Amsterdam, Department of Physiology, Amsterdam Cardiovascular Sciences, The Netherlands (M.S., L.M.D., J.v.d.V., D.W.D.K.).
Jiayi PeiDivision Heart and Lungs, Department of Cardiology (J.P., M.H., F.W.A.), University Medical Center Utrecht, The Netherlands.
Magdalena HarakalovaDivision Heart and Lungs, Department of Cardiology (J.P., M.H., F.W.A.), University Medical Center Utrecht, The Netherlands.
Larissa M DorschAmsterdam UMC, Vrije Universiteit Amsterdam, Department of Physiology, Amsterdam Cardiovascular Sciences, The Netherlands (M.S., L.M.D., J.v.d.V., D.W.D.K.).
Saskia SchlossarekInstitute of Experimental Pharmacology and Toxicology, Cardiovascular Research Center, University Medical Center Hamburg-Eppendorf, Germany (S.S., L.C.).
Michal MokryDepartment of Pediatric Gastroenterology, Wilhelmina Children's Hospital (M. Morky), University Medical Center Utrecht, The Netherlands.
Jaco C KnolAmsterdam UMC, Vrije Universiteit Amsterdam, Department of Medical Oncology, OncoProteomics Laboratory, VUmc-Cancer Center Amsterdam, The Netherlands (J.C.K., T.V.P., T.S., S.R.P., C.R.J.).
Thang V PhamAmsterdam UMC, Vrije Universiteit Amsterdam, Department of Medical Oncology, OncoProteomics Laboratory, VUmc-Cancer Center Amsterdam, The Netherlands (J.C.K., T.V.P., T.S., S.R.P., C.R.J.).
Tim SchelfhorstAmsterdam UMC, Vrije Universiteit Amsterdam, Department of Medical Oncology, OncoProteomics Laboratory, VUmc-Cancer Center Amsterdam, The Netherlands (J.C.K., T.V.P., T.S., S.R.P., C.R.J.).
Sander R PiersmaAmsterdam UMC, Vrije Universiteit Amsterdam, Department of Medical Oncology, OncoProteomics Laboratory, VUmc-Cancer Center Amsterdam, The Netherlands (J.C.K., T.V.P., T.S., S.R.P., C.R.J.).
Cris Dos RemediosSydney Heart Bank, Discipline of Anatomy, Bosch Institute, University of Sydney, Australia (C.d.R.).
Michiel DalinghausDepartment of Pediatric Cardiology (M.D.), Erasmus Medical Center Rotterdam, The Netherlands.
Michelle MichelsDepartment of Cardiology, Thorax Center (M. Michels), Erasmus Medical Center Rotterdam, The Netherlands.
Folkert W AsselbergsDivision Heart and Lungs, Department of Cardiology (J.P., M.H., F.W.A.), University Medical Center Utrecht, The Netherlands.
Marie-Jo MoutinGrenoble Institut des Neurosciences (GIN), Université Grenoble Alpes, Grenoble, France (M.-J.M.).
Lucie CarrierInstitute of Experimental Pharmacology and Toxicology, Cardiovascular Research Center, University Medical Center Hamburg-Eppendorf, Germany (S.S., L.C.).
Connie R JimenezAmsterdam UMC, Vrije Universiteit Amsterdam, Department of Medical Oncology, OncoProteomics Laboratory, VUmc-Cancer Center Amsterdam, The Netherlands (J.C.K., T.V.P., T.S., S.R.P., C.R.J.).
Jolanda van der Velden *Amsterdam UMC, Vrije Universiteit Amsterdam, Department of Physiology, Amsterdam Cardiovascular Sciences, The Netherlands (M.S., L.M.D., J.v.d.V., D.W.D.K.).
Diederik W D Kuster *Amsterdam UMC, Vrije Universiteit Amsterdam, Department of Physiology, Amsterdam Cardiovascular Sciences, The Netherlands (M.S., L.M.D., J.v.d.V., D.W.D.K.).
Vrije Universiteit Amsterdam · NLNetherlands Heart Institute · NLErasmus MC · NLUniversität Hamburg · DEGrenoble Institute of Neurosciences · FRRobert Bosch (Australia) · AUWilhelmina Children's Hospital · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHypertrophic cardiomyopathy (HCM) is the most common genetic heart disease. While ≈50% of patients with HCM carry a sarcomere gene mutation (sarcomere mutation-positive, HCM

methodsA proteomics screen was performed in cardiac tissue from 39 HCM

resultsIn all HCM patient samples, we found lower levels of metabolic pathway proteins and higher levels of extracellular matrix proteins. Levels of total and detyrosinated α-tubulin were markedly higher in HCM

conclusionsOur findings indicate that microtubules and especially its detyrosination contribute to the pathomechanism of patients with HCM

Indexed as

AdultAgedAnimalsCardiac MyosinsCardiomyopathy, HypertrophicCarrier ProteinsCase-Control StudiesDisease Models, AnimalFemaleHaploinsufficiencyHumansMaleMiddle AgedMyosin Binding Protein CMyosin Heavy ChainsProteomicsCardiac MyosinsCarrier ProteinsMYH7 protein, humanMyosin Binding Protein CMyosin Heavy ChainsTNNI3 protein, humanTNNT2 protein, humanTroponin ITroponin TTubulinTyrosinecardiomyopathiesgenotypeheart diseasesmutationproteomicstreatmenttubulin

Identifiers

PMID33430602
PMCPMC7819533
OpenAlexW3121093645

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.