Ruimin Ma
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Ruimin Ma has a total of 5 co-authors. Here are the top co-authors by number of shared publications:
- Di Sun
Department of Occupational Medicine and Toxicology, Clinical Center for Interstitial Lung Diseases, Beijing Institute of Respiratory Medicine, Beijing Chao-Yang Hospital, Capital Medical University , Beijing
1 shared publication - Nafeisa Dilixiati
Department of Occupational Medicine and Toxicology, Clinical Center for Interstitial Lung Diseases, Beijing Institute of Respiratory Medicine, Beijing Chao-Yang Hospital, Capital Medical University , Beijing
1 shared publication - Qiao Ye
Clinical Center for Interstitial Lung Diseases, Beijing Institute of Respiratory Medicine, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China
1 shared publication - Yawen Song
Department of Occupational Medicine and Toxicology, Clinical Center for Interstitial Lung Diseases, Beijing Institute of Respiratory Medicine, Beijing Chao-Yang Hospital, Capital Medical University , Beijing
1 shared publication - Yuanying Wang
Department of Respiratory and Critical Care Medicine, Beijing Institute of Respiratory Medicine and Beijing Chao‐Yang Hospital Capital Medical University Beijing China
1 shared publication
Latest Publications
- Open Access
- 23 March 2026
- Published by Oxford University Press (OUP) in American Journal of Respiratory Cell and Molecular Biology
- Vol. 74 (7) , 936-948
SPP1+ macrophages contribute to silica-induced pulmonary inflammation and fibrosis via the ERK/JNK signaling pathway
Secreted phosphoprotein 1-positive (SPP1+) macrophages play a critical role in the progression of silicosis, but their regulatory mechanisms remain unclear. In this study, we integrated single-cell RNA sequencing and spatial transcriptomics to characterize crucial macrophage subpopulations and their associated regulatory pathways during silicosis. Our results demonstrate that silica exposure significantly promotes the accumulation of SPP1+ macrophages within silicotic nodules. These macrophages contribute to inflammation by releasing pro-inflammatory cytokines such as TNF-α, MCP-1, and IL-6. Concurrently, they exhibit elevated ACTA2 RNA transcription levels, which enhance TGF-β production and drive fibrotic progression. These functional transitions are regulated by the ERK1/2 and JNK signaling pathways. Inhibition of SPP1 markedly attenuated silica-induced lung inflammation and fibrosis. Moreover, plasma SPP1 levels in silicosis patients were strongly correlated with disease onset and severity. Collectively, our findings indicate that SPP1+ macrophages are involved throughout the entire course of silicosis development, under the regulation of ERK/JNK signaling. Targeting SPP1+ macrophages may thus represent a promising therapeutic strategy for silicosis.
- 23 March 2026
- Published by Oxford University Press (OUP) in American Journal of Respiratory Cell and Molecular Biology
- Vol. 74 (7) , 936-948
Open AccessSPP1+ macrophages contribute to silica-induced pulmonary inflammation and fibrosis via the ERK/JNK signaling pathway
Secreted phosphoprotein 1-positive (SPP1+) macrophages play a critical role in the progression of silicosis, but their regulatory mechanisms remain unclear. In this study, we integrated single-cell RNA sequencing and spatial transcriptomics to characterize crucial macrophage subpopulations and their associated regulatory pathways during silicosis. Our results demonstrate that silica exposure significantly promotes the accumulation of SPP1+ macrophages within silicotic nodules. These macrophages contribute to inflammation by releasing pro-inflammatory cytokines such as TNF-α, MCP-1, and IL-6. Concurrently, they exhibit elevated ACTA2 RNA transcription levels, which enhance TGF-β production and drive fibrotic progression. These functional transitions are regulated by the ERK1/2 and JNK signaling pathways. Inhibition of SPP1 markedly attenuated silica-induced lung inflammation and fibrosis. Moreover, plasma SPP1 levels in silicosis patients were strongly correlated with disease onset and severity. Collectively, our findings indicate that SPP1+ macrophages are involved throughout the entire course of silicosis development, under the regulation of ERK/JNK signaling. Targeting SPP1+ macrophages may thus represent a promising therapeutic strategy for silicosis.