Evidence map›Paper›PMID 41993271›Full record

ArticlebioRxiv : the preprint server for biology2026

Longitudinal Single-Cell RNA-seq Profiling of Lung Cell Phenotypes, Signaling, and Cross-talk During Fibrosis Resolution.

Jennifer Speth, Vivian T Wong, Steve D Guzman, Yang Liu, Natalie M Walker, Rachel L Zemans, Timothy S Blackwell, Carlos A Aguilar, Marc Peters-Golden, Sean M Fortier

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Jennifer SpethDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109.
Vivian T WongDepartment of Biomedical Engineering, School of Engineering, University of Michigan.
Steve D GuzmanDepartment of Biomedical Engineering, School of Engineering, University of Michigan.
Yang LiuDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109.
Natalie M WalkerDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109.
Rachel L ZemansDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109.
Timothy S BlackwellDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109.
Carlos A AguilarDepartment of Biomedical Engineering, School of Engineering, University of Michigan.ORCID 0000-0003-3830-0634
Marc Peters-GoldenDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109.
Sean M FortierDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109.

Funding

Novel Functions of Lung Macrophages and Fibroblasts in Pulmonary Inflammation and FibrosisR35HL144979 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PETERS-GOLDEN, MARC L · 2019 to 2025
$6.5M
Mechanisms of Alveolar Homeostasis, Injury, Regeneration, and FibrosisR35HL160770 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Rachel Lynne Zemans · 2022 to 2026
$4.3M
Targeting dysfunctional epithelial repair in pulmonary fibrosisR01HL175555 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Timothy S. Blackwell · 2024 to 2026
$1.9M
Lung Myofibroblast De-Differentiation and Fibrosis Resolution Depend on cAMP-mediated Inhibition of HuR.K08HL163178 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Sean Michael Fortier · 2023 to 2026
$678k
NHLBI NIH HHS K08 HL163178NHLBI NIH HHS R01 HL175555NHLBI NIH HHS R35 HL144979NHLBI NIH HHS R35 HL160770
6 · The paper itself

Abstract

Resolution of fibrosis following lung injury is distinguished from persistent/progressive parenchymal scarring through the timely clearance of aberrant cell types, removal of excess collagens, and regeneration of alveolar structure. The requisite signaling pathways, cellular cross-talk, and phenotypic shifts associated with, and required for, resolution of established lung fibrosis have not been well characterized. To address this critical knowledge gap, we performed longitudinal single-cell RNA sequencing of whole mouse lung digests obtained during spontaneously resolving fibrosis. We observed a putatively pro-fibrotic macrophage population emerge during peak fibrosis and undergo partial clearance during resolution. Our study also revealed conspicuous shifts in well-established pathways associated with tissue repair and fibrosis among immune, mesenchymal, and epithelial cells during spontaneous resolution. In addition to a decline in pro-fibrotic driver pathways, the putative anti-fibrotic pathways cAMP, HGF/MET, and TWEAK were enriched in several cell types during spontaneous resolution. CellChat analysis was used to predict the cellular senders and recipients of each pathway and characterize their longitudinal changes. Our characterization of the cellular and molecular dynamics in whole lungs during spontaneous fibrosis resolution provides a foundation for the identification of endogenous pathways that might be leveraged to treat pulmonary fibrosis.

Identifiers

PMID41993271
PMCPMC13082050

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.