Evidence map›Paper›PMID 40121219›Full record

ArticleCell death discovery2025

Interplay between ALK2

Laura Coculo, Marius Wits, Irene Mariani, Giulia Fianco, Serena Cappato, Renata Bocciardi, Nicoletta Pedemonte, Elisabetta Volpe, Serena Ciolfi, Rosario Luigi Sessa and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

16 authors.

Laura CoculoInstitute of Molecular Biology and Pathology, National Research Council (CNR), Rome, Italy.
Marius WitsDepartment of Cell & Chemical Biology, Leiden University Medical Center (LUMC), Leiden, The Netherlands.ORCID http://orcid.org/0000-0003-1837-3481
Irene MarianiInstitute of Molecular Biology and Pathology, National Research Council (CNR), Rome, Italy.
Giulia FiancoInstitute of Molecular Biology and Pathology, National Research Council (CNR), Rome, Italy.
Serena CappatoUOC Genetica Medica, IRCCS Istituto Giannina Gaslini, Genoa, Italy.
Renata BocciardiUOC Genetica Medica, IRCCS Istituto Giannina Gaslini, Genoa, Italy.
Nicoletta PedemonteUOC Genetica Medica, IRCCS Istituto Giannina Gaslini, Genoa, Italy.
Elisabetta VolpeMolecular Neuroimmunology Unit, IRCCS Fondazione Santa Lucia, Rome, Italy.ORCID http://orcid.org/0000-0001-7985-2422
Serena CiolfiMolecular Neuroimmunology Unit, IRCCS Fondazione Santa Lucia, Rome, Italy.ORCID http://orcid.org/0009-0001-8378-9881
Rosario Luigi SessaInstitute of Molecular Biology and Pathology, National Research Council (CNR), Rome, Italy.
Serena RinaldoDepartment of Biochemical Sciences, Sapienza University of Rome, Rome, Italy.ORCID http://orcid.org/0000-0003-0682-023X
Francesca CutruzzolàDepartment of Biochemical Sciences, Sapienza University of Rome, Rome, Italy.ORCID http://orcid.org/0000-0002-4621-2135
Daniela TrisciuoglioInstitute of Molecular Biology and Pathology, National Research Council (CNR), Rome, Italy.ORCID http://orcid.org/0000-0002-7007-7914
Marie-Josè Goumans *Department of Cell & Chemical Biology, Leiden University Medical Center (LUMC), Leiden, The Netherlands.ORCID http://orcid.org/0000-0001-9344-6746
Gonzalo Sanchez-Duffhues *Department of Cell & Chemical Biology, Leiden University Medical Center (LUMC), Leiden, The Netherlands.
Venturina StagniInstitute of Molecular Biology and Pathology, National Research Council (CNR), Rome, Italy. venturina.stagni@cnr.it.ORCID http://orcid.org/0000-0002-3971-0398

Funding

Fondazione Telethon (Telethon Foundation) Seed Grant FOP GSA21A002Fondazione Telethon (Telethon Foundation) Seed Grant FOP-Renewal GSA23I001Ministero dell'Istruzione, dell'Università e della Ricerca (Ministry of Education, University and Research) PRIN202224M22R
6 · The paper itself

Abstract

Heterozygous mutations in the Bone morphogenetic protein (BMP) type I receptor ACVR1, encoding activin-like kinase 2 (ALK2), underlie all cases of the rare genetic musculoskeletal disorder Fibrodysplasia Ossificans Progressiva (FOP). The most commonly found mutant ALK2 p.R206H receptor variant exhibits loss of auto inhibition of BMP signaling and can be activated by Activins, while wild-type receptors remain unresponsive. Consequently, the downstream chondrogenic signaling is enhanced, thus driving heterotopic ossification within soft connective tissues. Despite several investigational treatments being evaluated in clinical trials, no cure for FOP exists today. The cellular and molecular mechanisms underlying disease progression are still being deciphered. In this study, we show a close interplay between the mutant ALK2

Identifiers

PMID40121219
PMCPMC11929866

What OpenQuestion holds

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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.