Mechanical stress promotes excessive NETs and exacerbates acute lung injury via Piezo1-mediated mitochondrial dysfunction.

Hangfei Jin, Yiwen Mei, Xi Gao, Wenwen Zhang, Heyue Li, Yitian Chen, Bingwei Sun

Abstract read

In one paragraph

Article in Redox biology, 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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5 · Who and what money

Authors and funding

7 authors.

Hangfei JinResearch Center for Neutrophil Engineering Technology, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou, Jiangsu Province, 215002, China.

Yiwen MeiResearch Center for Neutrophil Engineering Technology, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou, Jiangsu Province, 215002, China.

Xi GaoResearch Center for Neutrophil Engineering Technology, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou, Jiangsu Province, 215002, China.

Wenwen ZhangResearch Center for Neutrophil Engineering Technology, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou, Jiangsu Province, 215002, China.

Heyue LiResearch Center for Neutrophil Engineering Technology, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou, Jiangsu Province, 215002, China.

Yitian ChenResearch Center for Neutrophil Engineering Technology, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou, Jiangsu Province, 215002, China.

Bingwei SunResearch Center for Neutrophil Engineering Technology, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou, Jiangsu Province, 215002, China. Electronic address: sunbinwe@hotmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute lung injury (ALI) is a respiratory insufficiency syndrome precipitated by factors such as infection, sepsis, or systemic trauma. Excessive polymorphonuclear neutrophil (PMN) infiltration and activation represent the hallmark cellular features of early-stage ALI. However, it remains poorly understood how the pulmonary biomechanical microenvironment, remodeled by ALI-induced diffuse edema, decreased lung compliance, and mechanical ventilation, modulates PMN hyperactivation. Using a sequential model of LPS-induced lung injury and differential mechanical ventilation combined with an in vitro cell compression system, we demonstrate that PMN Piezo1 senses pathological physical strain and orchestrates pro-inflammatory responses. Single-cell RNA sequencing identified a mechanosensitive "mitochondrial-stress" PMN cluster that expands during ALI, defined by profound mitochondrial damage and elevated ROS production. Mechanistically, Piezo1 transduces mechanical stimuli into cytosolic Ca

Indexed as

Acute Lung InjuryExtracellular TrapsIon ChannelsMitochondriaStress, MechanicalAnimalsDisease Models, AnimalHumansLipopolysaccharidesMaleMiceNeutrophilsReactive Oxygen SpeciesIon ChannelsLipopolysaccharidesPIEZO1 protein, humanPiezo1 protein, mouseReactive Oxygen SpeciesAcute lung injuryMechanical stressNeutrophil extracellular traps (NETs)Piezo1Single-cell RNA sequencing

Identifiers

PMID42442116

DOI10.1016/j.redox.2026.104297

PMCPMC13382279

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LicenceCC BY-NC

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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 OpenQuestion graph.