Evidence map›Paper›PMID 37814319›Full record

ReviewJournal of translational medicine2023

Fibrosis and bone marrow: understanding causation and pathobiology.

Kanjaksha Ghosh, Durjoy K Shome, Bipin Kulkarni, Malay K Ghosh, Kinjalka Ghosh

Open access · goldAbstract readReview
In one paragraph

Review in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
9.0field-weighted citation impact, top 2% 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

24 citing papers in PubMed, 35 citations in OpenAlex.

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  8. EarlyCancers · 2025
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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

5 authors at 4 institutions in 2 countries.

Kanjaksha GhoshNational Institute of Immunohaematology, 13 Th Fl KEM Hospital, Parel, Mumbai, 400012, India. kanjakshaghosh@hotmail.com.ORCID http://orcid.org/0000-0002-0645-6565
Durjoy K ShomeDepartment of Pathophysiology, American University of Antigua College of Medicine, Coolidge, Antigua and Barbuda.
Bipin KulkarniDepartment of Molecular Biology and Haemostasis, National Institute of Immunohaematology, 13Th Fl KEM Hospital, Parel, Mumbai, 400012, India.
Malay K GhoshDepartment of Haematology, Nilratan Sarkar Medical College, Kolkata, 700014, West Bengal, India.
Kinjalka GhoshDepartment of Clinical Biochemistry, Tata Medical Centre and Homi Bhaba National Institute, Parel, Mumbai, 400012, India.
Homi Bhabha National Institute · INAmerican University of Antigua · AGICMR - National Institute of Immunohaemotology · INNil Ratan Sircar Medical College and Hospital · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone marrow fibrosis represents an important structural change in the marrow that interferes with some of its normal functions. The aetiopathogenesis of fibrosis is not well established except in its primary form. The present review consolidates current understanding of marrow fibrosis. We searched PubMed without time restriction using key words: bone marrow and fibrosis as the main stem against the terms: growth factors, cytokines and chemokines, morphology, megakaryocytes and platelets, myeloproliferative disorders, myelodysplastic syndrome, collagen biosynthesis, mesenchymal stem cells, vitamins and minerals and hormones, and mechanism of tissue fibrosis. Tissue marrow fibrosis-related papers were short listed and analysed for the review. It emerged that bone marrow fibrosis is the outcome of complex interactions between growth factors, cytokines, chemokines and hormones together with their facilitators and inhibitors. Fibrogenesis is initiated by mobilisation of special immunophenotypic subsets of mesenchymal stem cells in the marrow that transform into fibroblasts. Fibrogenic stimuli may arise from neoplastic haemopoietic or non-hematopoietic cells, as well as immune cells involved in infections and inflammatory conditions. Autoimmunity is involved in a small subset of patients with marrow fibrosis. Megakaryocytes and platelets are either directly involved or are important intermediaries in stimulating mesenchymal stem cells. MMPs, TIMPs, TGF-β, PDGRF, and basic FGF and CRCXL4 chemokines are involved in these processes. Genetic and epigenetic changes underlie many of these conditions.

Indexed as

Bone MarrowPrimary MyelofibrosisChemokinesCytokinesFibrosisHormonesHumansChemokinesCytokinesHormonesEpigeneticsHaemopoietic stem cellsMegakaryocytesMesenchymal stem cellsMyelofibrosisParathormoneSignal transductionTargeted therapy

Identifiers

PMID37814319
PMCPMC10561412
OpenAlexW4387451586

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.