Search Results - "Fortier, Sean M."

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  1. 1

    A Breath Fungal Secondary Metabolite Signature to Diagnose Invasive Aspergillosis by Koo, Sophia, Thomas, Horatio R., Daniels, S. David, Lynch, Robert C., Fortier, Sean M., Shea, Margaret M., Rearden, Preshious, Comolli, James C., Baden, Lindsey R., Marty, Francisco M.

    Published in Clinical infectious diseases (15-12-2014)
    “…Background. Invasive aspergillosis (IA) remains a leading cause of mortality in immunocompromised patients, in part due to the difficulty of diagnosing this…”
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    Journal Article
  2. 2

    Myofibroblast dedifferentiation proceeds via distinct transcriptomic and phenotypic transitions by Fortier, Sean M, Penke, Loka R, King, Dana, Pham, Tho X, Ligresti, Giovanni, Peters-Golden, Marc

    Published in JCI insight (22-03-2021)
    “…Myofibroblasts are the major cellular source of collagen, and their accumulation - via differentiation from fibroblasts and resistance to apoptosis - is a…”
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  3. 3

    KLF4 is a therapeutically tractable brake on fibroblast activation that promotes resolution of pulmonary fibrosis by Penke, Loka R, Speth, Jennifer M, Huang, Steven K, Fortier, Sean M, Baas, Jared, Peters-Golden, Marc

    Published in JCI insight (22-08-2022)
    “…There is a paucity of information about potential molecular brakes on the activation of fibroblasts that drive tissue fibrosis. The transcription factor…”
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    Journal Article
  4. 4

    Mechanical Stretch: An Important and Understudied Feature of Acute and Chronic Lung Injury by Cagino, Leigh M, Hensley, Matthew K, Fortier, Sean M, Dickson, Robert P

    “…Although the biochemical and immunological features of lung injury have been intensely studied in recent decades, the contributions of biophysical disruptions…”
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    Journal Article
  5. 5

    Illuminating the lung regenerative potential of prostanoids by Fortier, Sean M, Penke, Loka R, Peters-Golden, Marc

    Published in Science advances (25-03-2022)
    “…PGE and PGI receptors are potential targets for the treatment of chronic lung disease…”
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    Journal Article
  6. 6

    Prion Nucleation Site Unmasked by Transient Interaction with Phospholipid Cofactor by Zurawel, Ashley A, Walsh, Daniel J, Fortier, Sean M, Chidawanyika, Tamutenda, Sengupta, Suvrajit, Zilm, Kurt, Supattapone, Surachai

    Published in Biochemistry (Easton) (14-01-2014)
    “…Infectious mammalian prions can be formed de novo from purified recombinant prion protein (PrP) substrate through a pathway that requires the sequential…”
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  7. 7

    MAPK phosphatase 1 inhibition of p38[alpha] within lung myofibroblasts is essential for spontaneous fibrosis resolution by Fortier, Sean M, Walker, Natalie M, Penke, Loka R, Baas, Jared D, Shen, Qinxue, Speth, Jennifer M, Huang, Steven K, Zemans, Rachel L, Peters-Golden, Anton M. Bennetand Marc

    Published in The Journal of clinical investigation (15-05-2024)
    “…Fibrosis following tissue injury is distinguished from normal repair by the accumulation of pathogenic and apoptosis-resistant myofibroblasts (MFs), which…”
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    Journal Article
  8. 8

    MAPK phosphatase 1 inhibition of p38α within lung myofibroblasts is essential for spontaneous fibrosis resolution by Fortier, Sean M., Walker, Natalie M., Penke, Loka R., Baas, Jared D., Shen, Qinxue, Speth, Jennifer M., Huang, Steven K., Zemans, Rachel L., Bennett, Anton M., Peters-Golden, Marc

    Published in The Journal of clinical investigation (15-05-2024)
    “…Fibrosis following tissue injury is distinguished from normal repair by the accumulation of pathogenic and apoptosis-resistant myofibroblasts (MFs), which…”
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    Journal Article
  9. 9

    MAP kinase phosphatase-1 inhibition of p38α within lung myofibroblasts is essential for spontaneous fibrosis resolution by Fortier, Sean M, Walker, Natalie M, Penke, Loka R, Baas, Jared D, Shen, Qinxue, Speth, Jennifer M, Huang, Steven K, Zemans, Rachel L, Bennett, Anton M, Peters-Golden, Marc

    Published in The Journal of clinical investigation (21-03-2024)
    “…Fibrosis following tissue injury is distinguished from normal repair by the accumulation of pathogenic and apoptosis-resistant myofibroblasts (MFs), which…”
    Get full text
    Journal Article