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dc.creatorLin, Chih-Ru
dc.creatorBahmed, Karim
dc.creatorKosmider, Beata
dc.date.accessioned2022-09-01T16:19:32Z
dc.date.available2022-09-01T16:19:32Z
dc.date.issued2022-06-28
dc.identifier.citationLin C-R, Bahmed K, Kosmider B. Impaired Alveolar Re-Epithelialization in Pulmonary Emphysema. Cells. 2022; 11(13):2055. https://doi.org/10.3390/cells11132055
dc.identifier.issn2073-4409
dc.identifier.doihttp://dx.doi.org/10.34944/dspace/8109
dc.identifier.urihttp://hdl.handle.net/20.500.12613/8137
dc.description.abstractAlveolar type II (ATII) cells are progenitors in alveoli and can repair the alveolar epithelium after injury. They are intertwined with the microenvironment for alveolar epithelial cell homeostasis and re-epithelialization. A variety of ATII cell niches, transcription factors, mediators, and signaling pathways constitute a specific environment to regulate ATII cell function. Particularly, WNT/β-catenin, YAP/TAZ, NOTCH, TGF-β, and P53 signaling pathways are dynamically involved in ATII cell proliferation and differentiation, although there are still plenty of unknowns regarding the mechanism. However, an imbalance of alveolar cell death and proliferation was observed in patients with pulmonary emphysema, contributing to alveolar wall destruction and impaired gas exchange. Cigarette smoking causes oxidative stress and is the primary cause of this disease development. Aberrant inflammatory and oxidative stress responses result in loss of cell homeostasis and ATII cell dysfunction in emphysema. Here, we discuss the current understanding of alveolar re-epithelialization and altered reparative responses in the pathophysiology of this disease. Current therapeutics and emerging treatments, including cell therapies in clinical trials, are addressed as well.
dc.format.extent19 pages
dc.languageEnglish
dc.language.isoeng
dc.relation.ispartofFaculty/ Researcher Works
dc.relation.haspartCells, Vol. 11, No. 13
dc.relation.isreferencedbyMDPI
dc.rightsAttribution CC BY
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectAlveolar epithelium
dc.subjectAlveolar type II cells
dc.subjectEmphysema
dc.subjectTissue homeostasis
dc.subjectRegeneration
dc.subjectLung repair
dc.titleImpaired Alveolar Re-Epithelialization in Pulmonary Emphysema
dc.typeText
dc.type.genreJournal article
dc.contributor.groupCenter for Inflammation and Lung Research (Temple University)
dc.description.departmentMicrobiology, Immunology & Inflammation
dc.description.departmentThoracic Medicine and Surgery
dc.relation.doihttps://doi.org/10.3390/cells11132055
dc.ada.noteFor Americans with Disabilities Act (ADA) accommodation, including help with reading this content, please contact scholarshare@temple.edu
dc.description.schoolcollegeLewis Katz School of Medicine
dc.creator.orcidKosmider|0000-0001-7421-5424
dc.temple.creatorLin, Chih-Ru
dc.temple.creatorBahmed, Karim
dc.temple.creatorKosmider, Beata
refterms.dateFOA2022-09-01T16:19:32Z


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