Evidence map›Paper›PMID 33779513›Full record

ArticleAutophagy2021

TNF-induced necroptosis initiates early autophagy events via RIPK3-dependent AMPK activation, but inhibits late autophagy.

Wenxian Wu, Xiaojing Wang, Yadong Sun, Niklas Berleth, Jana Deitersen, David Schlütermann, Fabian Stuhldreier, Nora Wallot-Hieke, María José Mendiburo, Jan Cox and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Autophagy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
9.2field-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

57 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
  2. Article
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  4. Article
  5. NIBV Induces Incomplete Autophagy via AMPK-TFEB, Causing Kidney Injury in Chicks.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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  8. Review
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  17. Article
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  19. Review
  20. Cell Death Mechanisms inPathogens (Basel, Switzerland) · 2025
    Review
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

13 authors at 2 institutions in 1 country.

Wenxian WuInstitute of Molecular Medicine I, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.ORCID 0000-0003-4059-5945
Xiaojing WangInstitute of Molecular Medicine I, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
Yadong SunInstitute of Molecular Medicine I, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
Niklas BerlethInstitute of Molecular Medicine I, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
Jana DeitersenInstitute of Molecular Medicine I, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
David SchlütermannInstitute of Molecular Medicine I, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
Fabian StuhldreierInstitute of Molecular Medicine I, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
Nora Wallot-HiekeDWI-Leibniz Institute for Interactive Materials, Aachen, Germany.ORCID 0000-0003-4151-9557
María José MendiburoInstitute of Molecular Medicine I, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
Jan CoxInstitute of Molecular Medicine I, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.ORCID 0000-0002-7792-9374
Christoph PeterInstitute of Molecular Medicine I, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.ORCID 0000-0002-0048-2279
Ann Kathrin BergmannCore Facility for Electron Microscopy, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
Björn StorkInstitute of Molecular Medicine I, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.ORCID 0000-0002-4167-7806
Heinrich Heine University Düsseldorf · DEDWI – Leibniz Institute for Interactive Materials · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macroautophagy/autophagy and necroptosis represent two opposing cellular s tress responses. Whereas autophagy primarily fulfills a cyto-protective function, necroptosis is a form of regulated cell death induced via death receptors. Here, we aimed at investigating the molecular crosstalk between these two pathways. We observed that RIPK3 directly associates with AMPK and phosphorylates its catalytic subunit PRKAA1/2 at T183/T172. Activated AMPK then phosphorylates the autophagy-regulating proteins ULK1 and BECN1. However, the lysosomal degradation of autophagosomes is blocked by TNF-induced necroptosis. Specifically, we observed dysregulated SNARE complexes upon TNF treatment; e.g., reduced levels of full-length STX17. In summary, we identified RIPK3 as an AMPK-activating kinase and thus a direct link between autophagy- and necroptosis-regulating kinases.

Indexed as

AMP-Activated Protein KinasesAutophagyNecroptosisReceptor-Interacting Protein Serine-Threonine KinasesAnimalsClass III Phosphatidylinositol 3-KinasesFibroblastsMiceAMP-Activated Protein KinasesClass III Phosphatidylinositol 3-KinasesReceptor-Interacting Protein Serine-Threonine KinasesRipk3 protein, mouseAMPKautophagynecroptosisRIPK3STX17

Identifiers

PMID33779513
PMCPMC8726653
OpenAlexW3148063552

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.