ArticleProtein & cell2026
A cell differentiation landscape for monocyte and interstitial macrophage in the lung with diffuse alveolar damage.
Article in Protein & cell, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- MSCs/EVs-based therapy targeting DAD: research progress and future perspectives from ARDS and COVID-19 to RP-ILD.Stem cell research & therapy · 2026Review
- Dynamic orchestration of structural and immune cells in acuteFrontiers in immunology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Diffuse alveolar damage (DAD) is recognized as a deadly type of acute inflammatory lung injury caused by toxic inhalants, but its cellular and molecular pathogenesis remains largely unclear. In this study, by using a mouse model of ricin-induced DAD, we explored the heterogeneity of recruited monocyte (Mono) and Mono-derived interstitial macrophage (IM) in the DAD lung. There was the development of 2 distinct IM subsets, namely IMpi (pro-inflammatory) and IMai (anti-inflammatory), from recruited Monopi. A subset of recruited Monopi could get the proliferating phenotype (namely pMonopi), and meanwhile pMonopi served as the intermediate of Monopi-to-IMai transition. The presence of growth differentiation factor 15 (GDF15) facilitated Monopi-to-pMonopi-to-IMai transition, whereas GDF15 deficiency exerted the negative feedback effect of enhancing Monopi-to-IMpi shift. These findings provided a cell differentiation landscape for Mono and IM in the DAD lung, which would promote a deeper understanding of cellular immunology of DAD and offer a theoretical basis for developing novel therapeutic strategies against acute lung injury.
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Registered trials
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.