Evidence map›Paper›PMID 35561683›Full record

ArticleStem cell reports2022

Ripk3 signaling regulates HSCs during stress and represses radiation-induced leukemia in mice.

Lei Zhang, Huacheng Luo, Hong-Min Ni, Shanhui Liu, Hongyun Xing, Jun Zhang, Mark Sellin, Peter Breslin S J, Wei Wei, Mitchell F Denning and 4 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 20% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
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  5. Review
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  11. Science advances · 2023
    Article
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

14 authors at 4 institutions in 2 countries.

Lei ZhangDepartment of Cancer Biology, Oncology Research Institute, Cardinal Bernardin Cancer Center, Loyola University Chicago, Maywood, IL 60153, USA; Cyrus Tang Hematology Center, Collaborative Innovation Center of Hematology, National Clinical Research Center for Hematologic Diseases, Soochow University, Suzhou 215123, China.
Huacheng LuoDepartment of Pediatrics, Pennsylvania State University College of Medicine, Hershey, PA 17033, USA.
Hong-Min NiDepartment of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS 66160, USA.
Shanhui LiuDepartment of Cancer Biology, Oncology Research Institute, Cardinal Bernardin Cancer Center, Loyola University Chicago, Maywood, IL 60153, USA.
Hongyun XingDepartment of Cancer Biology, Oncology Research Institute, Cardinal Bernardin Cancer Center, Loyola University Chicago, Maywood, IL 60153, USA.
Jun ZhangDepartment of Biology, College of Life Sciences, Shanghai Normal University, Shanghai 200234, People's Republic of China.
Mark SellinDepartment of Cancer Biology, Oncology Research Institute, Cardinal Bernardin Cancer Center, Loyola University Chicago, Maywood, IL 60153, USA.
Peter Breslin S JDepartment of Cancer Biology, Oncology Research Institute, Cardinal Bernardin Cancer Center, Loyola University Chicago, Maywood, IL 60153, USA; Departments of Molecular/Cellular Physiology and Biology, Loyola University Chicago, Chicago, IL 60660, USA.
Wei WeiDepartment of Cancer Biology, Oncology Research Institute, Cardinal Bernardin Cancer Center, Loyola University Chicago, Maywood, IL 60153, USA.
Mitchell F DenningDepartment of Cancer Biology, Oncology Research Institute, Cardinal Bernardin Cancer Center, Loyola University Chicago, Maywood, IL 60153, USA.
William SmallDepartment of Radiation Oncology, Loyola University Medical Center, Maywood, IL 60153, USA.
Wen-Xing DingDepartment of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS 66160, USA.
Suming HuangDepartment of Pediatrics, Pennsylvania State University College of Medicine, Hershey, PA 17033, USA. Electronic address: shuang4@pennstatehealth.psu.edu.
Jiwang ZhangDepartment of Cancer Biology, Oncology Research Institute, Cardinal Bernardin Cancer Center, Loyola University Chicago, Maywood, IL 60153, USA; Department of Radiation Oncology, Loyola University Medical Center, Maywood, IL 60153, USA; Department of Pathology, Loyola University Medical Center, Maywood, IL 60153, USA. Electronic address: jzhang@luc.edu.
Loyola University Chicago · USLoyola University Medical Center · USPennsylvania State University · USUniversity of Kansas Medical Center · US

Funding

Mechanisms regulating autophagy in alcohol-induced liver injuryR01AA020518 · NIAAA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI DING, WEN-XING · 2011 to 2018
$2.3M
Autophagy in Alcoholic PancreatitisU01AA024733 · NIAAA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI DING, WEN-XING · 2017 to 2021
$1.7M
RIP1/RIP3-Calpain-Stat3 and NF-kappa B pathways in AML pathogenesis and treatmentR01CA223194 · NCI · LOYOLA UNIVERSITY CHICAGO · PI ZHANG, JIWANG · 2018 to 2022
$1.7M
Systematic identification of hematopoietic stem cell expansion factorsR01HL133560 · NHLBI · LOYOLA UNIVERSITY CHICAGO · PI ZHANG, JIWANG · 2017 to 2020
$1.5M
NCI NIH HHS R01 CA223194NHLBI NIH HHS R01 HL133560NIAAA NIH HHS R01 AA020518NIAAA NIH HHS U01 AA024733
6 · The paper itself

Abstract

Receptor-interacting protein kinase 3 (Ripk3) is one of the critical mediators of inflammatory cytokine-stimulated signaling. Here we show that Ripk3 signaling selectively regulates both the number and the function of hematopoietic stem cells (HSCs) during stress conditions. Ripk3 signaling is not required for normal homeostatic hematopoiesis. However, in response to serial transplantation, inactivation of Ripk3 signaling prevents stress-induced HSC exhaustion and functional HSC attenuation, while in response to fractionated low doses of ionizing radiation (IR), inactivation of Ripk3 signaling accelerates leukemia/lymphoma development. In both situations, Ripk3 signaling is primarily stimulated by tumor necrosis factor-α. Activated Ripk3 signaling promotes the elimination of HSCs during serial transplantation and pre-leukemia stem cells (pre-LSCs) during fractionated IR by inducing Mlkl-dependent necroptosis. Activated Ripk3 signaling also attenuates HSC functioning and represses a pre-LSC-to-LSC transformation by promoting Mlkl-independent senescence. Furthermore, we demonstrate that Ripk3 signaling induces senescence in HSCs and pre-LSCs by attenuating ISR-mediated mitochondrial quality control.

Indexed as

Leukemia, Radiation-InducedAnimalsHematopoietic Stem CellsMiceNecrosisProtein KinasesReceptor-Interacting Protein Serine-Threonine KinasesSignal TransductionProtein KinasesReceptor-Interacting Protein Serine-Threonine KinasesRipk3 protein, mouseHSCsionizing radiationleukemiaMlklnecroptosisRipk3

Identifiers

PMID35561683
PMCPMC9213819
OpenAlexW4280549284

What OpenQuestion holds

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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.