ReviewMolecular biology reports2026
The role of immune cell crosstalk and signaling pathways in the pathogenesis of pulmonary fibrosis.
Review in Molecular biology reports, 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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Authors and funding
6 authors.
Funding
Abstract
Pulmonary fibrosis is a category of progressive interstitial lung illnesses caused by atypical inflammatory healing mechanisms, marked by excessive fibroblast activation, aberrant myofibroblast development, and extracellular matrix (ECM) accumulation. Recent research has established that immune cell dysregulation and the aberrant activation of critical signaling pathways are pivotal in the initiation and advancement of fibrosis. Macrophages, neutrophils, dendritic cells, and natural killer (NK) cells collectively constitute a sophisticated innate immune network. M1/M2 polarization, NETs release, and immune surveillance failure are intricately linked to disease development. In adaptive immunity, CD4⁺ T cell subsets facilitate the shift from inflammation to fibrosis via Th1/Th2 imbalance, Th17 amplification, and phase-dependent Treg functionality. B cells aggravate tissue damage through autoantibodies, immunological complexes, and inflammatory cytokines, although regulatory B cells may provide protective effects during certain phases.The TGF-β/Smad signaling pathway is the principal axis of fibrosis, directly governing fibroblast transformation and extracellular matrix deposition. It establishes a highly interconnected signaling network involving pathways including NF-κB, JAK/STAT, and PI3K/AKT, enhancing inflammatory responses and pro-fibrotic effects. The pathogenic etiology of pulmonary fibrosis fundamentally entails immune dysregulation and aberrant tissue repair resulting from interactions between immune cells and signaling pathways. Subsequent investigations ought to amalgamate single-cell omics with spatial transcriptomics to systematically elucidate the spatiotemporal dynamics and essential signaling pathways of immunological subpopulations. This methodology will investigate innovative ways for multi-target combination interventions and microenvironment remodeling, with the objective of establishing theoretical foundations and translational significance for precision medicines in pulmonary fibrosis.
Indexed as
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41553576What Socratic holds
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 Socratic graph.