Evidence map›Paper›PMID 32155728›Full record

ReviewCells2020

Stress Erythropoiesis is a Key Inflammatory Response.

Robert F Paulson, Baiye Ruan, Siyang Hao, Yuanting Chen

Abstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
–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

69 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Physiological and Proteomic Responses to Chronic Stress and the Effects ofAnimals : an open access journal from MDPI · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Redox Modulation of Erythropoiesis by Selenoproteins.Biological trace element research · 2026
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

9 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.

Robert F PaulsonDepartment of Veterinary and Biomedical Sciences, Center for Molecular Immunology and Infectious Disease at Penn State University, University Park, PA 16802, USA.
Baiye RuanDepartment of Veterinary and Biomedical Sciences, Pathobiology Graduate Program at Penn State University, University Park, PA 16802, USA.
Siyang HaoDepartment of Veterinary and Biomedical Sciences, Graduate Program in Molecular, Cellular and Integrative Biosciences at Penn State University, University Park, PA 16802, USA.
Yuanting ChenDepartment of Veterinary and Biomedical Sciences, Graduate Program in Molecular, Cellular and Integrative Biosciences at Penn State University, University Park, PA 16802, USA.

Funding

The BMP4 dependent stress erythropoiesis pathway in short-term radioprotectionR01DK080040 · NIDDK · PENNSYLVANIA STATE UNIVERSITY, THE · PI PAULSON, ROBERT FRANK · 2009 to 2017
$2.6M
Selenium, Selenoproteins, and Stress ErythropoiesisR01DK119865 · NIDDK · PENNSYLVANIA STATE UNIVERSITY, THE · PI PAULSON, ROBERT FRANK, PRABHU, KUMBLE SANDEEP · 2019 to 2021
$1.1M
Metabolic Control of Erythroid DifferentiationR01HL146528 · NHLBI · PENNSYLVANIA STATE UNIVERSITY, THE · PI PAULSON, ROBERT FRANK · 2020 to 2022
$914k
NHLBI NIH HHS R01 HL146528NIDDK NIH HHS R01 DK080040NIDDK NIH HHS R01 DK119865
6 · The paper itself

Abstract

Bone marrow medullary erythropoiesis is primarily homeostatic. It produces new erythrocytes at a constant rate, which is balanced by the turnover of senescent erythrocytes by macrophages in the spleen. Despite the enormous capacity of the bone marrow to produce erythrocytes, there are times when it is unable to keep pace with erythroid demand. At these times stress erythropoiesis predominates. Stress erythropoiesis generates a large bolus of new erythrocytes to maintain homeostasis until steady state erythropoiesis can resume. In this review, we outline the mechanistic differences between stress erythropoiesis and steady state erythropoiesis and show that their responses to inflammation are complementary. We propose a new hypothesis that stress erythropoiesis is induced by inflammation and plays a key role in maintaining erythroid homeostasis during inflammatory responses.

Indexed as

AnimalsErythropoiesisHumansInflammationMiceStress, Physiologicalanemia of inflammationerythroblastic islandserythrophagocytosispro-inflammatory cytokinesstress erythropoiesis

Identifiers

PMID32155728
PMCPMC7140438

What OpenQuestion holds

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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.