Evidence map›Paper›PMID 31974657›Full record

ReviewCellular and molecular life sciences : CMLS2020

The mechanisms of pathological extramedullary hematopoiesis in diseases.

Xinxin Yang, Degao Chen, Haixia Long, Bo Zhu

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 2 pooled it
6.4field-weighted citation impact, top 3% 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

62 citing papers in PubMed, 2 syntheses or guidelines pooled it, 93 citations in OpenAlex.

  1. Pooled it
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  9. Galectin-9Aging cell · 2026
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2 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Xinxin YangInstitute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China.
Degao ChenInstitute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China.
Haixia LongInstitute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China. longhaixialhx@163.com.
Bo ZhuInstitute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China. bo.zhu@tmmu.edu.cn.ORCID http://orcid.org/0000-0003-0224-8512
Army Medical University · CN

Funding

National Natural Science Foundation of China 81472648National Natural Science Foundation of China 81620108023National Natural Science Foundation of China 81925030National Natural Science Foundation of China 81972699
6 · The paper itself

Abstract

Extramedullary hematopoiesis (EMH) is the expansion and differentiation of hematopoietic stem and progenitor cells outside of the bone marrow. In postnatal life, as a compensatory mechanism for ineffective hematopoiesis of the bone marrow, pathological EMH is triggered by hematopoietic disorders, insufficient hematopoietic compensation, and other pathological stress conditions, such as infection, advanced tumors, anemia, and metabolic stress. Pathological EMH has been reported in many organs, and the sites of pathological EMH may be related to reactivation of the embryonic hematopoietic structure in these organs. As a double-edged sword (blood and immune cell supplementation as well as clinical complications), pathological EMH has been widely studied in recent years. In particular, pathological EMH induced by late-stage tumors contributes to tumor immunosuppression. Thus, a deeper understanding of the mechanism of pathological EMH may be conducive to the development of therapies against the pathological processes that induce EMH. This article reviews the recent progress of research on the cellular and molecular mechanisms of pathological EMH in specific diseases.

Indexed as

Embryonic Stem CellsHematopoietic Stem CellsHematopoiesis, ExtramedullaryHumansImmunosuppression TherapyNeoplasmsStress, PhysiologicalAtherosclerosisErythropoiesisInflammationMyelofibrosisNicheThalassemia

Identifiers

PMID31974657
PMCPMC11104806
OpenAlexW3001823351

What Socratic holds

Textmetadata
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 Socratic graph.