---
title: "TARM1 promotes ARDS progression by driving M1 macrophage polarization"
id: "pubmed-42669243"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42669243"
content_type: "clinical_feed_article"
specialty: "Critical Care"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42669243/"
doi: "10.1016/j.bbrc.2026.154466"
published_at: "2026-10-08T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# TARM1 promotes ARDS progression by driving M1 macrophage polarization
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42669243
- **Specialty:** [Critical Care](https://medichelpline.com/clinical-feed/critical-care.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42669243/)
- **DOI:** [10.1016/j.bbrc.2026.154466](https://doi.org/10.1016%2Fj.bbrc.2026.154466)
- **Published At:** 2026-10-08T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- Background: Acute respiratory distress syndrome (**ARDS**) has incompletely defined pathophysiology. The study aimed to identify genes linked to ARDS and **M1 macrophage** polarization using public transcriptomic resources and experimental validation. - Data sources: Bulk transcriptomes from three independent murine ARDS models and single-cell RNA sequencing from ARDS lungs, all obtained from GEO (GSE193958, GSE216943, GSE263867, GSE217324). - Approach: Differential expression analysis across bulk datasets identified common genes; single-cell data identified genes enriched in M1 versus M2 macrophages; intersecting these sets produced candidate genes validated by qRT-PCR in ARDS mouse lungs. - Key candidate: **TARM1** emerged as a top hit, showing marked elevation in ARDS lung tissue and colocalization with the macrophage marker CD68. - In vitro findings: In LPS-stimulated RAW264.7 macrophages, TARM1 knockdown decreased pro‑inflammatory cytokine expression and attenuated LPS-induced **M1 macrophage** polarization. - In vivo findings: Macrophage-specific suppression of TARM1 using AAV6-mediated knockdown reduced lung wet-to-dry ratio, inflammatory cytokine levels, and histologic lung injury in ARDS models. - Interpretation: The data support a role for **TARM1** in promoting ARDS pathogenesis via regulation of macrophage M1 polarization; macrophage-targeted TARM1 inhibition mitigated experimental lung injury. - Limitations and provenance: All transcriptomic and single-cell datasets analyzed were from public GEO repositories; experiments were performed in murine models and in RAW264.7 cells. Details beyond those reported in the source (for example, numerical effect sizes, specific cytokines quantified, or precise experimental protocols) were not provided in the abstract.
## Clinical Analysis & Structured Key Points
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Epub 2026 Aug 29. # TARM1 may contribute to acute respiratory distress syndrome progression via regulating M1 macrophage polarization [Yu Chen](https://pubmed.ncbi.nlm.nih.gov/?term=Chen+Y&cauthor_id=42669243)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42669243/#full-view-affiliation-1 "The Second Clinical College of Chongqing Medical University, Chongqing, China."), [Daoxin Wang](https://pubmed.ncbi.nlm.nih.gov/?term=Wang+D&cauthor_id=42669243)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42669243/#full-view-affiliation-2 "The Second Clinical College of Chongqing Medical University, Chongqing, China. Electronic address: wangdaoxin@hospital.cqmu.edu.cn.") Affiliations Expand ### Affiliations * 1 The Second Clinical College of Chongqing Medical University, Chongqing, China. * 2 The Second Clinical College of Chongqing Medical University, Chongqing, China. Electronic address: wangdaoxin@hospital.cqmu.edu.cn. * PMID: **42669243** * DOI: [ 10.1016/j.bbrc.2026.154466 ](https://doi.org/10.1016/j.bbrc.2026.154466) Item in Clipboard # TARM1 may contribute to acute respiratory distress syndrome progression via regulating M1 macrophage polarization Yu Chen et al. Biochem Biophys Res Commun. 2026. Show details Display options Display options Format Abstract PubMed PMID Biochem Biophys Res Commun Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Biochem+Biophys+Res+Commun%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Biochem+Biophys+Res+Commun%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42669243/) . 2026 Oct 8:834:154466. doi: 10.1016/j.bbrc.2026.154466. Epub 2026 Aug 29. ### Authors [Yu Chen](https://pubmed.ncbi.nlm.nih.gov/?term=Chen+Y&cauthor_id=42669243)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42669243/#short-view-affiliation-1 "The Second Clinical College of Chongqing Medical University, Chongqing, China."), [Daoxin Wang](https://pubmed.ncbi.nlm.nih.gov/?term=Wang+D&cauthor_id=42669243)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42669243/#short-view-affiliation-2 "The Second Clinical College of Chongqing Medical University, Chongqing, China. Electronic address: wangdaoxin@hospital.cqmu.edu.cn.") ### Affiliations * 1 The Second Clinical College of Chongqing Medical University, Chongqing, China. * 2 The Second Clinical College of Chongqing Medical University, Chongqing, China. Electronic address: wangdaoxin@hospital.cqmu.edu.cn. * PMID: **42669243** * DOI: [ 10.1016/j.bbrc.2026.154466 ](https://doi.org/10.1016/j.bbrc.2026.154466) Item in Clipboard Full text links Cite Display options Display options Format Abstract PubMed PMID Linked Discoveries ## Abstract **Background:** The underlying pathophysiology of acute respiratory distress syndrome (ARDS), a potentially fatal condition, remains poorly understood. In this work, we screened important genes associated with ARDS and M1 macrophage polarization using publicly available bioinformatics datasets and experimental validation in an attempt to identify potential candidate genes for further investigation in ARDS. **Methods:** Bulk transcriptomic data from three independent murine ARDS models were analyzed to identify common differentially expressed genes. Single-cell RNA sequencing data from ARDS lungs were used to identify genes differentially expressed between M1 and M2 macrophages. Candidate genes were obtained by intersecting these two gene sets and were validated by qRT-PCR in the lungs of ARDS mice. The top candidate, TARM1, was further investigated in LPS-stimulated RAW264.7 macrophages and in vivo through macrophage-specific AAV6-mediated knockdown. **Results:** One important potential gene, TARM1, was markedly elevated in ARDS lung tissue and colocalized with the macrophage marker CD68. TARM1 knockdown in vitro reduced pro-inflammatory cytokine expression and LPS-induced M1 macrophage polarization. In vivo, macrophage-specific TARM1 suppression reduced the lung wet-to-dry ratio, inflammatory cytokine levels, and lung damage. **Conclusions:** TARM1 may promote ARDS pathogenesis by regulating macrophage M1 polarization. Macrophage-specific TARM1 inhibition alleviates lung injury, suggesting that TARM1 may be a potential target for further research in ARDS. All transcriptomic and single-cell data analyzed in this study were obtained from public GEO repositories (GSE193958, GSE216943, GSE263867, and GSE217324). **Keywords:** ARDS; Lung injury; M1 macrophages; Macrophage polarization; TARM1. Copyright © 2026 Elsevier Inc. All rights reserved. [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. ## Similar articles * [_CD274_ (PD-L1) negatively regulates M1 macrophage polarization in ALI/ARDS. ](https://pubmed.ncbi.nlm.nih.gov/38440722/) Tang N, Yang Y, Xie Y, Yang G, Wang Q, Li C, Liu Z, Huang JA.Tang N, et al.Front Immunol. 2024 Feb 19;15:1344805. doi: 10.3389/fimmu.2024.1344805. eCollection 2024.Front Immunol. 2024.PMID: 38440722Free PMC article. * [ hnRNPA2B1 promotes the production of exosomal miR-103-3p from endothelial progenitor cells to alleviate macrophage M1 polarization in acute respiratory distress syndrome. ](https://pubmed.ncbi.nlm.nih.gov/40381491/) Yang L, Chen T, Huang Y, Yang Y, Cheng X, Wei F.Yang L, et al.Int Immunopharmacol. 2025 Jun 17;158:114830. doi: 10.1016/j.intimp.2025.114830. Epub 2025 May 17.Int Immunopharmacol. 2025.PMID: 40381491 * [_IFIH1_ Contributes to M1 Macrophage Polarization in ARDS. ](https://pubmed.ncbi.nlm.nih.gov/33519803/) Zhang S, Chu C, Wu Z, Liu F, Xie J, Yang Y, Qiu H.Zhang S, et al.Front Immunol. 2021 Jan 14;11:580838. doi: 10.3389/fimmu.2020.580838. eCollection 2020.Front Immunol. 2021.PMID: 33519803Free PMC article. * [ IFIH1/IRF1/STAT1 promotes sepsis associated inflammatory lung injury via activating macrophage M1 polarization. ](https://pubmed.ncbi.nlm.nih.gov/36462334/) Wang A, Kang X, Wang J, Zhang S.Wang A, et al.Int Immunopharmacol. 2023 Jan;114:109478. doi: 10.1016/j.intimp.2022.109478. Epub 2022 Nov 30.Int Immunopharmacol. 2023.PMID: 36462334Free PMC article. * [ Natural Compounds Regulate Macrophage Polarization and Alleviate Inflammation Against ALI/ARDS. ](https://pubmed.ncbi.nlm.nih.gov/40001495/) Yin Z, Song R, Yu T, Fu Y, Ding Y, Nie H.Yin Z, et al.Biomolecules. 2025 Jan 29;15(2):192. doi: 10.3390/biom15020192.Biomolecules. 2025.PMID: 40001495Free PMC article.Review. 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