ReviewFrontiers in immunology2025
Chemokines as key mediators in RIPI: pathophysiology and translational potential.
Review in Frontiers in immunology, 2025. 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
Radiation-induced pulmonary injury (RIPI) is a common adverse effect following thoracic radiotherapy (RT), and immune-related responses play a pivotal role in the pathogenesis of RIPI. Chemokines are important components of the human immune system which could modulate inflammatory responses. Their levels fluctuate following radiation. These chemokines recruit relevant immune cells, such as macrophages and lymphocytes, and induce lung inflammatory responses. In addition to early-stage inflammation, chemokines are also associated with radiation-induced pulmonary fibrosis (RIPF) at a late stage and can augment the risk of post-radiation lung metastasis. Because of the correlation between chemokines and RIPI, chemokines may be useful for RIPI diagnosis and treatment. This review aims to summarize the alterations of the levels of different chemokines after radiation, the regulatory mechanisms, and the advancements of research on the diagnosis and treatment of RIPI by chemokines, in order to provide references for the subsequent RIPI research.
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