ReviewFrontiers in immunology2026
Research progress on molecular mechanisms and signaling pathways of toxic metal exposure-induced lung fibrosis.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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Abstract
Toxic metal exposure is a pressing global health concern, with accumulating evidence linking it to the onset and progression of pulmonary fibrosis. Mechanistically, metal-induced pulmonary fibrosis operates through a complex, interconnected signaling network rather than a single linear cascade. The initiating role of oxidative stress and the central hub function of the transforming growth factor-β/Smad (TGF-β/Smad) pathway are well-established, whereas the contributions of non-canonical mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt), Janus kinase/signal transducer and activator of transcription (JAK/STAT), and mammalian target of rapamycin complex 1 (mTORC1) pathways are supported by varying degrees of preclinical evidence, with some crosstalk mechanisms remaining largely hypothetical. Concurrently, persistent Toll-like receptor 4/nuclear factor kappa-B/NOD-like receptor family pyrin domain containing 3 (TLR4/NF-κB/NLRP3)-driven inflammation, macrophage polarization imbalance, impaired autophagy-lysosomal function, and non-apoptotic cell death pathways including ferroptosis and pyroptosis collectively promote alveolar epithelial injury, fibroblast-to-myofibroblast transition, and excessive extracellular matrix deposition. We summarize current therapeutic strategies-ranging from antioxidant/anti-inflammatory agents and TGF-β/autophagy modulators to metal chelators and emerging stem cell/nanomedicine approaches-and highlight their preclinical promise and translational challenges. Major unresolved issues include the translational gap between animal models and real-world human exposure scenarios, controversies over mixed-metal dose-response thresholds, and insufficient understanding of feedback and compensatory mechanisms within the molecular network. We outline future research directions aimed at bridging these gaps, with the goal of establishing a comprehensive theoretical framework for early warning, precision diagnosis, and targeted intervention in toxic metal-related pulmonary fibrosis.
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