<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wei YY</submitter><funding>Anhui Medical University</funding><funding>National Natural Science Foundation of China</funding><funding>research and practice innovation project of graduate students of Anhui Medical University</funding><funding>clinical medical research and transformation project of Anhui Province</funding><pagination>1717-1743</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12283003</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>21(8)</volume><pubmed_abstract>Microplastics (MPs) induce mitochondrial dysfunction and iron accumulation, contributing to mitochondrial macroautophagy/autophagy and ferroptosis, which has increased susceptibility to the exacerbation of chronic obstructive pulmonary disease (COPD); however, the underlying mechanism remains unclear. We demonstrated that MPs intensified inflammation in COPD by enhancing autophagy-dependent ferroptosis (ADF) in vitro and in vivo. In the lung tissues of patients with COPD, the concentrations of MPs, especially polystyrene microplastics (PS-MPs), were significantly higher than that of the control group, as detected by pyrolysis gas chromatography mass spectrometry (Py-GCMS), with increased iron accumulation. The exposure to PS-MPs, 2 μm in size, resulted in their being deposited in the lungs</pubmed_abstract><journal>Autophagy</journal><pubmed_title>Microplastics exacerbate ferroptosis via mitochondrial reactive oxygen species-mediated autophagy in chronic obstructive pulmonary disease.</pubmed_title><pmcid>PMC12283003</pmcid><funding_grant_id>YJS20230121</funding_grant_id><funding_grant_id>202304295107020038</funding_grant_id><funding_grant_id>82170050</funding_grant_id><pubmed_authors>Wei YY</pubmed_authors><pubmed_authors>Zhang DW</pubmed_authors><pubmed_authors>Chen KG</pubmed_authors><pubmed_authors>Fei GH</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Li F</pubmed_authors><pubmed_authors>Wang MY</pubmed_authors><pubmed_authors>Chen TT</pubmed_authors><pubmed_authors>Zhang L</pubmed_authors><pubmed_authors>Ding YC</pubmed_authors></additional><is_claimable>false</is_claimable><name>Microplastics exacerbate ferroptosis via mitochondrial reactive oxygen species-mediated autophagy in chronic obstructive pulmonary disease.</name><description>Microplastics (MPs) induce mitochondrial dysfunction and iron accumulation, contributing to mitochondrial macroautophagy/autophagy and ferroptosis, which has increased susceptibility to the exacerbation of chronic obstructive pulmonary disease (COPD); however, the underlying mechanism remains unclear. We demonstrated that MPs intensified inflammation in COPD by enhancing autophagy-dependent ferroptosis (ADF) in vitro and in vivo. In the lung tissues of patients with COPD, the concentrations of MPs, especially polystyrene microplastics (PS-MPs), were significantly higher than that of the control group, as detected by pyrolysis gas chromatography mass spectrometry (Py-GCMS), with increased iron accumulation. The exposure to PS-MPs, 2 μm in size, resulted in their being deposited in the lungs</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Aug</publication><modification>2026-03-31T10:31:52.742Z</modification><creation>2025-08-23T03:09:21.766Z</creation></dates><accession>S-EPMC12283003</accession><cross_references><pubmed>40114310</pubmed><doi>10.1080/15548627.2025.2481126</doi></cross_references></HashMap>