Evidence map›Paper›PMID 42733072›Full record

ArticleNature communications2026

Inhibition of RhoA-mediated secretory autophagy in megakaryocytes mitigates myelofibrosis in mice.

Isabelle C Becker, Siobhan Branfield, Maria N Barrachina, Virginia Camacho, Joshua Lykins, Andrew P Stone, Ethan Walsey, Muhammad Bennani, Bernadette A Chua, Robert A J Signer and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors.

Isabelle C BeckerVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA. i.becker@qmul.ac.uk.ORCID http://orcid.org/0000-0003-2725-8493
Siobhan BranfieldVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Maria N BarrachinaVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Virginia CamachoVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Joshua LykinsDepartment of Molecular and Cellular Biochemistry, University of Kentucky College of Medicine, Lexington, KY, USA.
Andrew P StoneVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Ethan WalseyVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Muhammad BennaniVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Bernadette A ChuaDivision of Regenerative Medicine, Department of Medicine, Stem Cell Discovery Center, Sanford Stem Cell Institute, Moores Cancer Center, University of California San Diego, La Jolla, CA, USA.
Robert A J SignerDivision of Regenerative Medicine, Department of Medicine, Stem Cell Discovery Center, Sanford Stem Cell Institute, Moores Cancer Center, University of California San Diego, La Jolla, CA, USA.
Kellie R MachlusVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.ORCID http://orcid.org/0000-0002-2155-1050
Sidney W WhiteheartDepartment of Molecular and Cellular Biochemistry, University of Kentucky College of Medicine, Lexington, KY, USA.
Harvey G RowethDivision of Hematology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.ORCID http://orcid.org/0000-0002-1100-8409
Joseph E ItalianoVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA. Joseph.italiano@childrens.harvard.edu.ORCID http://orcid.org/0000-0001-6547-9663

Funding

The Centrosome as a master controller of platelet production.R35HL161175 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI JOSEPH E ITALIANO · 2022 to 2026
$5.3M
Deutsche Forschungsgemeinschaft (German Research Foundation) BE 7766/2-1NHLBI NIH HHS R35 HL161175U.S. Department of Health & Human Services | National Institutes of Health (NIH) R35HL161175
6 · The paper itself

Abstract

Megakaryocytes (MKs) are polyploid cells that maintain bone marrow homeostasis by secreting cytokines, including transforming growth factor β1 (TGFβ1). During neoplastic transformation, MKs accumulate in the bone marrow, promoting fibrotic remodeling that leads to myelofibrosis. However, the therapeutic potential of targeting MK cytokine secretion remains poorly understood. Because unconventional secretion of TGFβ1 and interleukin 1β (IL1β) via secretory autophagy occurs in other cell types, we investigated whether MKs may utilize the same mechanism. Disrupting secretory autophagy, or inhibiting the small GTPase RhoA or its downstream effector Rho-associated kinase (ROCK), markedly reduced TGFβ1 and IL1β secretion in vitro. Conditional deletion of the autophagy gene Atg5 in the hematopoietic system limited megakaryocytosis and aberrant cytokine secretion in an MPL

Indexed as

AutophagyMegakaryocytesPrimary MyelofibrosisrhoA GTP-Binding Proteinrho GTP-Binding ProteinsAnimalsAutophagy-Related Protein 5FemaleHumansInterleukin-1betaJanus Kinase 2MaleMiceMice, Inbred C57BLMice, Knockoutrho-Associated KinasesAtg5 protein, mouseAutophagy-Related Protein 5Interleukin-1betaJak2 protein, mouseJanus Kinase 2rhoA GTP-Binding ProteinRhoA protein, mouserho-Associated Kinasesrho GTP-Binding ProteinsTransforming Growth Factor beta1

Identifiers

PMID42733072
PMCPMC13572371

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.