Evidence map›Paper›PMID 41663041›Full record

ArticleThe Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation2026

Spatial transcriptomics reveals coordinated endothelial and epithelial activator protein-1 activation in chronic lung allograft dysfunction.

Yasufumi Goda, Tatsuhiko Naito, Mudassir M Banday, Andrew S Potter, Igor Odintsov, Kapil Patel, Nicole Davis, Stefi Lee, Amit Gaggar, Ivan Rosas and 3 more

Abstract read
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In one paragraph

Article in The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

13 authors.

Yasufumi GodaDivision of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Tatsuhiko NaitoDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY.
Mudassir M BandayDivision of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Andrew S PotterDivision of Pulmonary Medicine and Heart Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, OH.
Igor OdintsovDivision of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Kapil PatelDepartment of Medicine,Tampa General Hospital, Tampa, FL.
Nicole DavisDepartment of Medicine,Tampa General Hospital, Tampa, FL.
Stefi LeeDivision of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Amit GaggarDivision of Pulmonary, Allergy and Critical Care Medicine University of Alabama at Birmingham, Birmingham, AL.
Ivan RosasDivision of Pulmonary, Critical Care, and Sleep Medicine, Baylor College of Medicine, Houston, TX.
Gabriel LoorDivision of Cardiothoracic Transplantation and Circulatory Support, Baylor College of Medicine, Houston, TX.
Don HayesDivision of Pulmonary Medicine and Heart Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, OH.
Nirmal S SharmaDivision of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; Division of Pulmonary, Critical Care, and Sleep Medicine, Baylor College of Medicine, Houston, TX. Electronic address: nirmal.sharma@bcm.edu.

Funding

Microbial Dysbiosis in Chronic Lung Allograft DysfunctionR01HL161620 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI Nirmal S Sharma · 2022 to 2026
$2.6M
NHLBI NIH HHS R01 HL161620
6 · The paper itself

Abstract

Chronic lung allograft dysfunction (CLAD) limits long-term lung graft survival, yet its specific gene expression profiles remain unclear. We performed comprehensive spatial transcriptomic analyses of human lungs from CLAD patients, non-CLAD transplant recipients, and non-transplanted controls. In CLAD, AP-1 target genes, including JUNB and FOS, were significantly upregulated in both the epithelium and endothelium, whereas anti-fibrotic genes such as A2M and surfactant proteins (SFTPA1,2) were upregulated in non-CLAD. The lymphocyte population in CLAD was predominantly composed of T cells, with elevated JAK3-IL7R signaling. TNF and IL-17 signaling pathways were commonly activated in both the epithelium and endothelium, with JUNB and FOS serving as central hubs within pro-inflammatory, pro-fibrotic gene networks. These findings suggest that coordinated AP-1 activation and shared inflammatory and fibrotic signaling across epithelial and endothelial compartments may drive CLAD. Our results highlight the transcriptionally active roles of both compartments and provide new mechanistic insights into CLAD pathogenesis.

Indexed as

Lung TransplantationPrimary Graft DysfunctionTranscription Factor AP-1TranscriptomeAllograftsChronic DiseaseFemaleGene Expression ProfilingGraft RejectionHumansMaleMiddle AgedSignal TransductionSpatial TranscriptomicsTranscription Factor AP-1Activator protein-1Chronic lung allograft dysfunctionFibrogenesisIL-17Lung transplantationSpatial transcriptomics

Identifiers

PMID41663041
PMCPMC13274917

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.