Evidence map›Paper›PMID 39810777›Full record

ReviewKidney international reports2025

Targeting the Type I Interferon Pathway in Glomerular Kidney Disease: Rationale and Therapeutic Opportunities.

James Tumlin, Brad Rovin, Hans-Joachim Anders, Eduardo F Mysler, David R W Jayne, Tsutomu Takeuchi, Catharina Lindholm, Gudrun Weiss, Alessandro Sorrentino, Kevin Woollard and 1 more

Abstract readReview
In one paragraph

Review in Kidney international reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

  1. Trial
  2. Trial
  3. Article
  4. Review
  5. 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

11 authors.

James TumlinNephroNet Clinical Trials Consortium, Buford, Georgia, USA.
Brad RovinDepartment of Internal Medicine, The Ohio State University Wexner Medical Center, Columbus, Ohio, USA.
Hans-Joachim AndersDivision of Nephrology, Department of Medicine IV, University Hospital, Ludwig-Maximilians-University Munich, Munich, Germany.
Eduardo F MyslerOrganizacion Medica de Investigación, Buenos Aires, Argentina.
David R W JayneDepartment of Medicine, University of Cambridge, Cambridge, UK.
Tsutomu TakeuchiDepartment of Rheumatology and Applied Immunology, Saitama Medical University and Division of Rheumatology, Department of Internal Medicine, Keio University, Tokyo, Japan.
Catharina LindholmBioPharmaceuticals R&D, AstraZeneca R&D, Gothenburg, Sweden.
Gudrun WeissGlobal Medical Affairs, Respiratory and Immunology, BioPharmaceuticals Medical, AstraZeneca, Cambridge, UK.
Alessandro SorrentinoGlobal Medical Affairs, Respiratory and Immunology, BioPharmaceuticals Medical, AstraZeneca, Cambridge, UK.
Kevin WoollardBioscience Renal, Research and Early Development, Cardiovascular, Renal and Metabolism, BioPharmaceuticals R&D, AstraZeneca, Cambridge, UK.
Nicola FerrariTranslational Science and Experimental Medicine, Early R&I, BioPharmaceuticals R&D, AstraZeneca, Cambridge, UK.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type I interferons (IFNs) are immunostimulatory molecules that can activate the innate and adaptive immune systems. In cases of immune dysfunction, prolonged activation of the type I IFN pathway has been correlated with kidney tissue damage in a wide range of kidney disorders, such as lupus nephritis (LN) and focal segmental glomerulosclerosis (FSGS). Genetic mutations, such as

Indexed as

anifrolumabimmune dysfunctioninterferon pathwaykidney diseaselupus nephritistype I interferon

Identifiers

PMID39810777
PMCPMC11725820

What OpenQuestion holds

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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.