Evidence map›Paper›PMID 42624116›Full record

ArticleCell genomics2026

Cell-type-specific damage scores reveal kidney and liver disease trajectories in single-cell and spatial transcriptomics.

Tsimafei Padvitski, Paula Unger Avila, He Chen, Cem Özel, Fabian Braun, Marie-Kristin Kroll, Christian Vossen, Peter Wienand, Linus Butt, David Unnersjö-Jess and 12 more

Abstract read
In one paragraph

Article in Cell genomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

22 authors.

Tsimafei PadvitskiCologne Excellence Cluster on Cellular Stress Responses in Age-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, North Rhine-Westphalia, Germany.
Paula Unger AvilaCologne Excellence Cluster on Cellular Stress Responses in Age-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, North Rhine-Westphalia, Germany.
He ChenDepartment II of Internal Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, 50937 Cologne, North Rhine-Westphalia, Germany; Center for Molecular Medicine Cologne, Faculty of Medicine and University Hospital Cologne, University of Cologne, 50931 Cologne, North Rhine-Westphalia, Germany.
Cem ÖzelDepartment II of Internal Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, 50937 Cologne, North Rhine-Westphalia, Germany; Center for Molecular Medicine Cologne, Faculty of Medicine and University Hospital Cologne, University of Cologne, 50931 Cologne, North Rhine-Westphalia, Germany.
Fabian BraunIII. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, 20246 Hamburg, Germany; Hamburg Center for Kidney Health, University Medical Center Hamburg-Eppendorf, Hamburg, 20246 Hamburg, Germany; Martin Zeitz Center for Rare Diseases, University Medical Center Hamburg-Eppendorf, Hamburg, 20246 Hamburg, Germany.
Marie-Kristin KrollDepartment II of Internal Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, 50937 Cologne, North Rhine-Westphalia, Germany; Center for Molecular Medicine Cologne, Faculty of Medicine and University Hospital Cologne, University of Cologne, 50931 Cologne, North Rhine-Westphalia, Germany.
Christian VossenMax Planck Institute for Metabolism Research, 50931 Cologne, North Rhine-Westphalia, Germany.
Peter WienandMax Planck Institute for Metabolism Research, 50931 Cologne, North Rhine-Westphalia, Germany.
Linus ButtDepartment II of Internal Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, 50937 Cologne, North Rhine-Westphalia, Germany; Center for Molecular Medicine Cologne, Faculty of Medicine and University Hospital Cologne, University of Cologne, 50931 Cologne, North Rhine-Westphalia, Germany.
David Unnersjö-JessDepartment II of Internal Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, 50937 Cologne, North Rhine-Westphalia, Germany; Center for Molecular Medicine Cologne, Faculty of Medicine and University Hospital Cologne, University of Cologne, 50931 Cologne, North Rhine-Westphalia, Germany; Science for Life Laboratory, Department of Applied Physics, Royal Institute of Technology, 17165 Solna, Stockholm County, Sweden.
Anna-Lena SchumacherMax Planck Institute for Biology of Aging, 50931 Cologne, North Rhine-Westphalia, Germany.
Kat Folz-DonahueMax Planck Institute for Biology of Aging, 50931 Cologne, North Rhine-Westphalia, Germany.
Heike GöbelInstitute of Pathology, University Hospital of Cologne, 50937 Cologne, North Rhine-Westphalia, Germany.
Christoph KuppeDivision of Nephrology and Clinical Immunology, RWTH Aachen University, 52074 Aachen, North Rhine-Westphalia, Germany.
Roman-Ulrich MüllerCologne Excellence Cluster on Cellular Stress Responses in Age-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, North Rhine-Westphalia, Germany; Department II of Internal Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, 50937 Cologne, North Rhine-Westphalia, Germany; Center for Molecular Medicine Cologne, Faculty of Medicine and University Hospital Cologne, University of Cologne, 50931 Cologne, North Rhine-Westphalia, Germany.
Pål Olof WestermarkWorking Group Husbandry & Health, Research Institute for Farm Animal Biology (FBN), 18196 Dummerstorf, Mecklenburg-Vorpommern, Germany; Institute for Biostatistics and Informatics in Medicine and Ageing Research, Rostock University Medical Center, 18057 Rostock, Mecklenburg-Vorpommern, Germany.
Paul Thomas BrinkkötterDepartment II of Internal Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, 50937 Cologne, North Rhine-Westphalia, Germany; Center for Molecular Medicine Cologne, Faculty of Medicine and University Hospital Cologne, University of Cologne, 50931 Cologne, North Rhine-Westphalia, Germany.
Bernhard SchermerCologne Excellence Cluster on Cellular Stress Responses in Age-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, North Rhine-Westphalia, Germany; Department II of Internal Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, 50937 Cologne, North Rhine-Westphalia, Germany; Center for Molecular Medicine Cologne, Faculty of Medicine and University Hospital Cologne, University of Cologne, 50931 Cologne, North Rhine-Westphalia, Germany.
Thomas BenzingCologne Excellence Cluster on Cellular Stress Responses in Age-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, North Rhine-Westphalia, Germany; Department II of Internal Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, 50937 Cologne, North Rhine-Westphalia, Germany; Center for Molecular Medicine Cologne, Faculty of Medicine and University Hospital Cologne, University of Cologne, 50931 Cologne, North Rhine-Westphalia, Germany.
Frank Thomas WunderlichMax Planck Institute for Metabolism Research, 50931 Cologne, North Rhine-Westphalia, Germany.
Martin KannDepartment II of Internal Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, 50937 Cologne, North Rhine-Westphalia, Germany; Center for Molecular Medicine Cologne, Faculty of Medicine and University Hospital Cologne, University of Cologne, 50931 Cologne, North Rhine-Westphalia, Germany. Electronic address: martin.kann@uk-koeln.de.
Andreas BeyerCologne Excellence Cluster on Cellular Stress Responses in Age-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, North Rhine-Westphalia, Germany; Center for Molecular Medicine Cologne, Faculty of Medicine and University Hospital Cologne, University of Cologne, 50931 Cologne, North Rhine-Westphalia, Germany; Institute for Genetics, Faculty of Mathematics and Natural Sciences, University of Cologne, 50931 Cologne, North Rhine-Westphalia, Germany. Electronic address: andreas.beyer@uni-koeln.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Degenerative diseases progress through gradual cell-intrinsic damage that is difficult to resolve with bulk transcriptomics or discrete cell-state analysis. We introduce a generalizable single-cell and spatial transcriptomics framework that quantifies continuous damage trajectories in vivo using cell-type-specific scores. Applied to chronic kidney disease and metabolic dysfunction-associated steatotic liver disease, the podocyte damage score (PDS) and hepatocyte damage score (HDS) place individual podocytes and hepatocytes on a health-to-damage axis. Across mouse and human single-cell RNA sequencing (scRNA-seq), single-nucleus RNA-seq (snRNA-seq), spatial transcriptomics, proteomics, histology, and clinical datasets, PDS and HDS robustly detect disease-associated damage, align disease models as well as unperturbed cells, and reveal conserved pathways. The PDS links podocyte injury and FSGS progression to circadian gene-expression disruption. The HDS identifies a damage threshold in metabolic dysfunction-associated steatotic liver disease (MASLD)/NASH beyond which hepatocytes adopt senescent, metabolically dysfunctional states. These damage scores enable scalable mapping of degenerative disease progression and stage-specific therapeutic targets.

Indexed as

Liver DiseasesSingle-Cell AnalysisTranscriptomeAnimalsHepatocytesHumansMicePodocytesSingle-Cell Gene Expression AnalysisSpatial Transcriptomicscellular damagecircadian rhythmdegenerative diseaseFSGShepatocyteMASLDpodocytesenescencesingle-cell RNA sequencingspatial transcriptomics

Identifiers

PMID42624116
PMCPMC13689510

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