Article in Nature communications, 2024. 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.
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
18 authors.
Kiyoka Saito *International Research Center for Medical Sciences, Kumamoto University, Kumamoto, Japan.
Mark van der Garde *Division of Molecular Medicine and Gene Therapy, Lund Stem Cell Center, Lund University, Lund, Sweden.
Terumasa UmemotoInternational Research Center for Medical Sciences, Kumamoto University, Kumamoto, Japan.ORCID 0000-0003-0423-9003
Natsumi MiharadaInternational Research Center for Medical Sciences, Kumamoto University, Kumamoto, Japan.ORCID 0000-0001-6989-5314
Julia SjöbergDivision of Molecular Medicine and Gene Therapy, Lund Stem Cell Center, Lund University, Lund, Sweden.ORCID 0000-0002-0400-2025
Valgardur SigurdssonDivision of Molecular Medicine and Gene Therapy, Lund Stem Cell Center, Lund University, Lund, Sweden.
Haruki ShirozuInternational Research Center for Medical Sciences, Kumamoto University, Kumamoto, Japan.
Shunsuke KameiDivision of Molecular and Vascular Biology, Institute of Resource Development and Analysis, Kumamoto University, Kumamoto, Japan.
Visnja RadulovicDivision of Molecular Medicine and Gene Therapy, Lund Stem Cell Center, Lund University, Lund, Sweden.
Mitsuyoshi SuzukiDivision of Molecular Medicine and Gene Therapy, Lund Stem Cell Center, Lund University, Lund, Sweden.ORCID 0000-0002-9969-3454
Satoshi NakanoDivision of Molecular Medicine and Gene Therapy, Lund Stem Cell Center, Lund University, Lund, Sweden.
Stefan LangStemTherapy Bioinformatics Core facility, Lund Stem Cell Center, Lund University, Lund, Sweden.ORCID 0000-0002-0854-2328
Jenny HanssonDivision of Molecular Hematology, Lund Stem Cell Center, Lund University, Lund, Sweden.ORCID 0000-0001-9174-8089
Martin L OlssonDivision of Hematology and Transfusion Medicine, Lund University, Lund, Sweden.ORCID 0000-0003-1647-9610
Takashi MinamiDivision of Molecular and Vascular Biology, Institute of Resource Development and Analysis, Kumamoto University, Kumamoto, Japan.ORCID 0000-0002-2345-1379
Gunnar GourasDepartment of Experimental Medical Sciences, Lund University, Lund, Sweden.ORCID 0000-0002-5500-6325
Johan FlygareDivision of Molecular Medicine and Gene Therapy, Lund Stem Cell Center, Lund University, Lund, Sweden.ORCID 0000-0002-1962-5276
Kenichi MiharadaInternational Research Center for Medical Sciences, Kumamoto University, Kumamoto, Japan. kenmiharada@kumamoto-u.ac.jp.ORCID 0000-0001-8073-4001
Funding
No grant is acknowledged in the PubMed record.
6 · The paper itself
Abstract
Hematopoietic stem cells (HSCs) react to various stress conditions. However, it is unclear whether and how HSCs respond to severe anemia. Here, we demonstrate that upon induction of acute anemia, HSCs rapidly proliferate and enhance their erythroid differentiation potential. In severe anemia, lipoprotein profiles largely change and the concentration of ApoE increases. In HSCs, transcription levels of lipid metabolism-related genes, such as very low-density lipoprotein receptor (Vldlr), are upregulated. Stimulation of HSCs with ApoE enhances their erythroid potential, whereas HSCs in Apoe knockout mice do not respond to anemia induction. Vldlr
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.
Lipoprotein metabolism mediates hematopoietic stem cell responses under acute anemic conditions. · full record | OpenQuestion