ArticleTranslational oncology2019
Serological Assessment of Activated Fibroblasts by alpha-Smooth Muscle Actin (α-SMA): A Noninvasive Biomarker of Activated Fibroblasts in Lung Disorders.
Article in Translational oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 82 citations in OpenAlex.
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- Piezo1 promote macrophage-to-myofibroblast transition and bladder fibrosis in neurogenic bladder.World journal of urology · 2026Article
- Matrix viscoelasticity regulates dermal fibroblast activation in a three-dimensional fibrillar microenvironment.bioRxiv : the preprint server for biology · 2026Article
- Modulation of NF-κB and cytokine signaling byFrontiers in pharmacology · 2026Article
- Design and Synthesis of Novel Pirfenidone Analogues for Targeting Fibroblast Differentiation via Transforming Growth Factor-β/Smad Pathway UsingACS pharmacology & translational science · 2025Article
- Targeting JNK1/2 and P38 Mitogen-Activated Protein Kinases With Pazopanib Mitigates Bleomycin-Induced Lung Fibrosis.Archiv der Pharmazie · 2025Article
- Distinct lung functional, histological and cell senescence signatures in the single and repetitive bleomycin mouse models of idiopathic pulmonary fibrosis.Physiological reports · 2025Article
- Effect of CTMP1 gene on pulmonary fibrosis.Toxicological research · 2025Article
- Mechanisms of breast cancer metastasis: the role of extracellular matrix.Molecular and cellular biochemistry · 2025Review
- Nano-drug delivery strategies affecting cancer-associated fibroblasts to reduce tumor metastasis.Acta pharmaceutica Sinica. B · 2025Review
- Article
- MicroRNAs as promising drug delivery target to ameliorate chronic obstructive pulmonary disease using nano-carriers: a comprehensive review.Molecular and cellular biochemistry · 2025Review
- Targeting fibroblast-endothelial cell interactions in LAM pathogenesis using 3D spheroid models and spatial transcriptomics.JCI insight · 2025Article
- Airway remodeling in chronic obstructive pulmonary disease: characteristics and opportunities.Frontiers in medicine · 2025Review
- Targeting Fibroblast-Endothelial Interactions in LAM Pathogenesis: 3D Spheroid and Spatial Transcriptomic Insights for Therapeutic Innovation.bioRxiv : the preprint server for biology · 2024Article
- Human amniotic membrane modulates collagen production and deposition in vitro.Scientific reports · 2024Article
- Transformation of macrophages into myofibroblasts in fibrosis-related diseases: emerging biological concepts and potential mechanism.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesRemodeling of the extracellular matrix (ECM) is a key event in different lung disorders, such as fibrosis and cancer. The most common cell type in the connective tissue is fibroblasts, which transdifferentiate into myofibroblasts upon activation. All myofibroblasts express α-SMA, which has been found to be upregulated in lung fibrosis and cancer. We evaluated the potential of α-SMA as a noninvasive biomarker of activated fibroblasts in lung fibrosis and cancer.
methodsA monoclonal antibody was raised against the N-terminal of α-SMA, and a novel competitive enzyme-linked immunosorbent assay (ELISA) measuring α-SMA was developed and technically characterized. Levels of α-SMA were measured in the fibroblast model, "scar-in-a-jar", and in serum from patients with idiopathic pulmonary fibrosis (IPF), chronic obstructive lung disorder (COPD) and non-small cell lung cancer (NSCLC) belonging to two different cohorts.
resultsThe novel α-SMA assay was developed and validated as technically robust. Based on the scar-in-a-jar results, α-SMA was only present in the fibroblasts activated by TGF-β. In cohort 1, levels of α-SMA were significantly higher in IPF, COPD and NSCLC patients compared to healthy controls (P = 0.04, P = 0.001 and P <0.0001, respectively). The area under the receiver operating characteristics (AUROC) for separation of healthy controls from IPF patients was 0.865, healthy controls from COPD patients was 0.892 and healthy controls from NSCLC patients was 0.983. In cohort 2, levels of α-SMA were also significantly higher in NSCLC patients compared to healthy controls (P = 0) and the AUROC for separating NSCLC and healthy controls was 0.715.
conclusionsIn this study we developed and validated a robust competitive ELISA assay targeting the N-terminal of α-SMA. The level of α-SMA was upregulated when adding TGF-β, indicating that α-SMA is increased in activated fibroblasts. The level of α-SMA in circulation was significantly higher in patients with IPF, COPD and NSCLC compared to healthy controls. This assay could potentially be used as a novel noninvasive serological biomarker for lung disorders by providing a surrogate measure of activated fibroblasts.
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Registered trials
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