Evidence map›Paper›PMID 29371597›Full record

ReviewCell death & disease2018

Immunological consequences of kidney cell death.

Maysa Sarhan, Anne von Mässenhausen, Christian Hugo, Rainer Oberbauer, Andreas Linkermann

Open access · goldAbstract readReview
In one paragraph

Review in Cell death & disease, 2018. 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
3.7field-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

57 citing papers in PubMed, 105 citations in OpenAlex.

  1. Article
  2. Article
  3. Research progress on the mechanism of FOXO protein in sepsis.Apoptosis : an international journal on programmed cell death · 2026
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. The complexities of cell death mechanisms: a new perspective in systemic sclerosis therapy.Apoptosis : an international journal on programmed cell death · 2025
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Role of necroptosis in kidney health and disease.Nature reviews. Nephrology · 2023
    Review
  16. Review
  17. Review
  18. Review
  19. Review
  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

5 authors at 3 institutions in 2 countries.

Maysa SarhanDivision of Nephrology and Dialysis, Department of Medicine III, Medical University Vienna, Vienna, Austria.
Anne von MässenhausenDivision of Nephrology, Department of Internal Medicine III, University Hospital Carl Gustav Carus at the Technische Universität Dresden, Dresden, Germany.
Christian HugoDivision of Nephrology, Department of Internal Medicine III, University Hospital Carl Gustav Carus at the Technische Universität Dresden, Dresden, Germany.
Rainer OberbauerDivision of Nephrology and Dialysis, Department of Medicine III, Medical University Vienna, Vienna, Austria.
Andreas LinkermannDivision of Nephrology, Department of Internal Medicine III, University Hospital Carl Gustav Carus at the Technische Universität Dresden, Dresden, Germany. andreas.linkermann@uniklinikum-dresden.de.
Medical University of Vienna · ATTU Dresden · DEUniversity Hospital Carl Gustav Carus · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Death of renal cells is central to the pathophysiology of acute tubular necrosis, autoimmunity, necrotizing glomerulonephritis, cystic kidney disease, urosepsis, delayed graft function and transplant rejection. By means of regulated necrosis, immunogenic damage-associated molecular patterns (DAMPs) and highly reactive organelles such as lysosomes, peroxisomes and mitochondria are released from the dying cells, thereby causing an overwhelming immunologic response. The rupture of the plasma membrane exhibits the "point of no return" for the immunogenicity of regulated cell death, explaining why apoptosis, a highly organized cell death subroutine with long-lasting plasma membrane integrity, elicits hardly any immune response. Ferroptosis, an iron-dependent necrotic type cell death, results in the release of DAMPs and large amounts of lipid peroxides. In contrast, anti-inflammatory cytokines are actively released from cells that die by necroptosis, limiting the DAMP-induced immune response to a surrounding microenvironment, whereas at the same time, inflammasome-associated caspases drive maturation of intracellularly expressed interleukin-1β (IL-1β). In a distinct setting, additionally interleukin-18 (IL-18) is expressed during pyroptosis, initiated by gasdermin-mediated plasma membrane rupture. As all of these pathways are druggable, we provide an overview of regulated necrosis in kidney diseases with a focus on immunogenicity and potential therapeutic interventions.

Indexed as

AnimalsApoptosisAutoimmunityHumansKidneyModels, BiologicalNecrosisSignal Transduction

Identifiers

PMID29371597
PMCPMC5833784
OpenAlexW2788311271

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.