Evidence map›Paper›PMID 34654937›Full record

ReviewCellular and molecular life sciences : CMLS2021

RIPK3 signaling and its role in the pathogenesis of cancers.

Shanhui Liu, Kanak Joshi, Mitchell F Denning, Jiwang Zhang

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. RIPK3 Orchestrates Scar-Associated Macrophage Dysfunction to Drive Pulmonary Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Pathogens (Basel, Switzerland) · 2025
    Article
  15. Review
  16. The Role of N6-Methyladenosine in Mitochondrial Dysfunction and Pathology.International journal of molecular sciences · 2025
    Review
  17. Article
  18. Article
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Shanhui Liu *Department of Cancer Biology, Oncology Institute, Cardinal Bernardin Cancer Center, Loyola University Medical Center, Maywood, IL, 60153, USA.ORCID http://orcid.org/0000-0001-9254-5339
Kanak Joshi *Department of Cancer Biology, Oncology Institute, Cardinal Bernardin Cancer Center, Loyola University Medical Center, Maywood, IL, 60153, USA.
Mitchell F DenningDepartment of Cancer Biology, Oncology Institute, Cardinal Bernardin Cancer Center, Loyola University Medical Center, Maywood, IL, 60153, USA.
Jiwang ZhangDepartment of Cancer Biology, Oncology Institute, Cardinal Bernardin Cancer Center, Loyola University Medical Center, Maywood, IL, 60153, USA. jzhang@luc.edu.
Loyola University Medical Center · US

Funding

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 HL133560rip1/rip3-calpain-stat3 and nf-kappa b pathways in aml pathogenesis and treatment R01 CA223194-01systematic identification of hematopoietic stem cell expansion factors R01 HL133560-01
6 · The paper itself

Abstract

RIPK3 (receptor-interacting protein kinase 3) is a serine/threonine-protein kinase. As a key component of necrosomes, RIPK3 is an essential mediator of inflammatory factors (such as TNFα-tumor necrosis factor α) and infection-induced necroptosis, a programmed necrosis. In addition, RIPK3 signaling is also involved in the regulation of apoptosis, cytokine/chemokine production, mitochondrial metabolism, autophagy, and cell proliferation by interacting with and/or phosphorylating the critical regulators of the corresponding signaling pathways. Similar to apoptosis, RIPK3-signaling-mediated necroptosis is inactivated in most types of cancers, suggesting RIPK3 might play a critical suppressive role in the pathogenesis of cancers. However, in some inflammatory types of cancers, such as pancreatic cancers and colorectal cancers, RIPK3 signaling might promote cancer development by stimulating proliferation signaling in tumor cells and inducing an immunosuppressive response in the tumor environment. In this review, we summarize recent research progress in the regulators of RIPK3 signaling, and discuss the function of this pathway in the regulation of mixed lineage kinase domain-like (MLKL)-mediated necroptosis and MLKL-independent cellular behaviors. In addition, we deliberate the potential roles of RIPK3 signaling in the pathogenesis of different types of cancers and discuss the potential strategies for targeting this pathway in cancer therapy.

Indexed as

ApoptosisAutophagyCell ProliferationChemokinesHumansMitochondriaNecroptosisNeoplasmsProtein KinasesReceptor-Interacting Protein Serine-Threonine KinasesSignal TransductionChemokinesMLKL protein, humanProtein KinasesReceptor-Interacting Protein Serine-Threonine KinasesRIPK3 protein, humanCancer pathogenesisMLKL-independent signalingMLKL necroptosisRIPK3 signaling

Identifiers

PMID34654937
PMCPMC9044760
OpenAlexW3206728688

What OpenQuestion holds

Textmetadata
LicenceTDM
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.