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Bruce D. Uhal
Researcher at Michigan State University
Publications - 129
Citations - 6554
Bruce D. Uhal is an academic researcher from Michigan State University. The author has contributed to research in topics: Angiotensin II & Lung. The author has an hindex of 39, co-authored 118 publications receiving 5686 citations. Previous affiliations of Bruce D. Uhal include Cardiovascular Institute of the South & University of Illinois at Chicago.
Papers
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Journal ArticleDOI
Upregulation of gelatinases A and B, collagenases 1 and 2, and increased parenchymal cell death in COPD.
Lourdes Segura-Valdez,Annie Pardo,Miguel Gaxiola,Bruce D. Uhal,Carina Becerril,Moisés Selman +5 more
TL;DR: Findings suggest that there is an upregulation of collagenase 1 and 2 and gelatinases A and B, and an increase in endothelial and epithelial cell death, which may contribute to the pathogenesis of COPD through the remodeling of airways and alveolar structures.
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Fibroblasts from idiopathic pulmonary fibrosis and normal lungs differ in growth rate, apoptosis, and tissue inhibitor of metalloproteinases expression.
Carlos A. Ramos,Martha Montaño,Jorge Garcia-Alvarez,Victor Ruiz,Bruce D. Uhal,Moises Selman,Annie Pardo +6 more
TL;DR: It is suggested that fibroblasts from IPF exhibit a profibrotic secretory phenotype, with lower growth rate and increased spontaneous apoptosis, which is similar to that seen in control lungs.
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Alveolar epithelial cell death adjacent to underlying myofibroblasts in advanced fibrotic human lung
TL;DR: It is demonstrated that the cuboidal epithelium of the fibrotic lung contains dying as well as proliferating cells and support the hypothesis that alveolar epithelial cell death is induced by abnormal lung fibroblasts in vivo as it is in vitro.
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ACE2, Much More Than Just a Receptor for SARS-COV-2.
Lobelia Samavati,Bruce D. Uhal +1 more
TL;DR: The potential of exploiting the modulation of ACE2/ MAS pathway as a natural protection of lung injury by modulation ofACE2/MAS axis or by developing targeted drugs to inhibit proteases required for viral entry is speculated.
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Abrogation of bleomycin-induced epithelial apoptosis and lung fibrosis by captopril or by a caspase inhibitor.
TL;DR: The data suggest that the efficacy of captopril to inhibit experimental lung fibrogenesis is related to inhibition of apoptosis and the antifibrotic potential of a caspase inhibitor is demonstrated.