{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Sharma S"],"funding":["NIH HHS"],"pagination":["501-512"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8830451"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["28(4)"],"pubmed_abstract":["Mitochondrial quality control is sustained by Miro1 (Rhot1), a calcium-binding membrane-anchored GTPase during mitophagy. The exact mechanism that operates the interaction of Miro1 with mitophagy machinery and their role in cigarette smoke (CS)-induced mitochondrial dysfunction that often results in lung inflammation is unclear. We hypothesized that Miro1 plays an important role in regulating mitophagy machinery and the resulting lung inflammation by CS exposure to mice. The lung epithelial Rhot1<sup>fl/fl</sup> (WT) and Rhot1<sup>CreCC10</sup> mice were exposed to mainstream CS for 3 days (acute) and 4 months (chronic). Acute CS exposure showed a notable increase in the total inflammatory cells, macrophages, and neutrophils that are associated with inflammatory mediators. Chronic exposure"],"journal":["Pathophysiology : the official journal of the International Society for Pathophysiology"],"pubmed_title":["Epithelial Ablation of Miro1/Rhot1 GTPase Augments Lung Inflammation by Cigarette Smoke."],"pmcid":["PMC8830451"],"funding_grant_id":["The National Institutes of Health (NIH) 1R01HL135613, R01 ES029177, HL137738, and R01 HL133404"],"pubmed_authors":["Muthumalage T","Sharma S","Wang Q","Rahman I"],"additional_accession":[]},"is_claimable":false,"name":"Epithelial Ablation of Miro1/Rhot1 GTPase Augments Lung Inflammation by Cigarette Smoke.","description":"Mitochondrial quality control is sustained by Miro1 (Rhot1), a calcium-binding membrane-anchored GTPase during mitophagy. The exact mechanism that operates the interaction of Miro1 with mitophagy machinery and their role in cigarette smoke (CS)-induced mitochondrial dysfunction that often results in lung inflammation is unclear. We hypothesized that Miro1 plays an important role in regulating mitophagy machinery and the resulting lung inflammation by CS exposure to mice. The lung epithelial Rhot1<sup>fl/fl</sup> (WT) and Rhot1<sup>CreCC10</sup> mice were exposed to mainstream CS for 3 days (acute) and 4 months (chronic). Acute CS exposure showed a notable increase in the total inflammatory cells, macrophages, and neutrophils that are associated with inflammatory mediators. Chronic exposure","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Nov","modification":"2025-04-26T03:50:45.818Z","creation":"2025-04-06T10:59:14.288Z"},"accession":"S-EPMC8830451","cross_references":{"pubmed":["35366248"],"doi":["10.3390/pathophysiology28040033"]}}