Evidence map›Paper›PMID 27895645›Full record

ReviewFrontiers in immunology2016

Inflamm-Aging of Hematopoiesis, Hematopoietic Stem Cells, and the Bone Marrow Microenvironment.

Larisa V Kovtonyuk, Kristin Fritsch, Xiaomin Feng, Markus G Manz, Hitoshi Takizawa

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 245 papers.

0numbers the graph read from it
0cells of the map it votes in
245citing papers in PubMed
19.1field-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

245 citing papers in PubMed, 353 citations in OpenAlex.

  1. Trial
  2. Review
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  7. The immunology behind inflammaging-causes, sources, and mechanisms.The Journal of allergy and clinical immunology · 2026
    Review
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  9. Review
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  12. Review
  13. Article
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  17. Mathematical modeling ofProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  18. A RANKLBone research · 2026
    Article
  19. Review
  20. Article

185 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

5 authors at 3 institutions in 2 countries.

Larisa V KovtonyukDivision of Hematology, University Hospital Zurich, University of Zurich , Zurich , Switzerland.
Kristin FritschDivision of Hematology, University Hospital Zurich, University of Zurich , Zurich , Switzerland.
Xiaomin FengInternational Research Center for Medical Sciences , Kumamoto , Japan.
Markus G ManzDivision of Hematology, University Hospital Zurich, University of Zurich , Zurich , Switzerland.
Hitoshi TakizawaInternational Research Center for Medical Sciences , Kumamoto , Japan.
Kumamoto Medical Center · JPUniversity Hospital of Zurich · CHUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

All hematopoietic and immune cells are continuously generated by hematopoietic stem cells (HSCs) and hematopoietic progenitor cells (HPCs) through highly organized process of stepwise lineage commitment. In the steady state, HSCs are mostly quiescent, while HPCs are actively proliferating and contributing to daily hematopoiesis. In response to hematopoietic challenges, e.g., life-threatening blood loss, infection, and inflammation, HSCs can be activated to proliferate and engage in blood formation. The HSC activation induced by hematopoietic demand is mediated by direct or indirect sensing mechanisms involving pattern recognition receptors or cytokine/chemokine receptors. In contrast to the hematopoietic challenges with obvious clinical symptoms, how the aging process, which involves low-grade chronic inflammation, impacts hematopoiesis remains undefined. Herein, we summarize recent findings pertaining to functional alternations of hematopoiesis, HSCs, and the bone marrow (BM) microenvironment during the processes of aging and inflammation and highlight some common cellular and molecular changes during the processes that influence hematopoiesis and its cells of origin, HSCs and HPCs, as well as the BM microenvironment. We also discuss how age-dependent alterations of the immune system lead to subclinical inflammatory states and how inflammatory signaling might be involved in hematopoietic aging. Our aim is to present evidence supporting the concept of "Inflamm-Aging," or inflammation-associated aging of hematopoiesis.

Indexed as

ageingcytokinehematopoietic stem cellinflammationnichepathogen recognition receptor

Identifiers

PMID27895645
PMCPMC5107568
OpenAlexW2553708507

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.