ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2026
Piezo1-specific deletion in macrophage attenuates radiation-induced lung injury progression in mice.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 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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Abstract
backgroundMacrophages play a crucial role in the inflammation and wound repair processes of radiation-induced lung injury (RILI). The mechanosensitive ion channel Piezo1 is upregulated during these inflammatory and wound repair processes. However, the involvement of macrophage Piezo1 in the pathogenesis of RILI remains unclear. This study aims to elucidate the regulatory role of Piezo1 in the injury and repair process in RILI and to investigate the underlying mechanisms.
methodsWe established Myeloid-specific knockout of Piezo1 (Piezo1
resultsOur findings revealed that Piezo1 is upregulated in lung macrophages in mice with RILI. Myeloid Piezo1 knockout provided protective effects in mice with RILI. Myeloid-specific Piezo1 deficiency alleviates inflammatory responses, manifested by the alleviation of inflammatory damage in lung tissue, changes in the concentrations of related inflammatory factors. Simultaneously, this deficiency reduces radiation-induced pulmonary fibrosis, with improved fibrosis indicators and decreased expression of EMT markers. Moreover, myeloid Piezo1 knockout inhibited paracrine-induced EMT of BEAS-2B cells by alveolar macrophages, and reduced macrophage recruitment. Mechanistically, the regulatory effects of Piezo1 on lung macrophages were activated Ca
conclusionOur findings revealed the important function of Piezo1 in RILI, knockout or pharmacological inhibition of Piezo1may serve as a promising strategy for treating RILI.
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