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  1. Article ; Online: Fibroblast heterogeneity in pulmonary fibrosis: a new target for therapeutics development?

    Tsoyi, Konstantin / Rosas, Ivan O

    The European respiratory journal

    2024  Volume 63, Issue 2

    MeSH term(s) Humans ; Pulmonary Fibrosis/pathology ; Myofibroblasts ; Lung/pathology ; Fibroblasts/pathology
    Language English
    Publishing date 2024-02-08
    Publishing country England
    Document type Editorial ; Comment
    ZDB-ID 639359-7
    ISSN 1399-3003 ; 0903-1936
    ISSN (online) 1399-3003
    ISSN 0903-1936
    DOI 10.1183/13993003.02188-2023
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  2. Article ; Online: Defining the Genetic Landscape of Idiopathic Pulmonary Fibrosis: Role of Common and Rare Variants.

    Moss, Benjamin J / Rosas, Ivan O

    American journal of respiratory and critical care medicine

    2023  Volume 207, Issue 9, Page(s) 1118–1120

    MeSH term(s) Humans ; Idiopathic Pulmonary Fibrosis/genetics ; Genetic Predisposition to Disease
    Language English
    Publishing date 2023-02-16
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 1180953-x
    ISSN 1535-4970 ; 0003-0805 ; 1073-449X
    ISSN (online) 1535-4970
    ISSN 0003-0805 ; 1073-449X
    DOI 10.1164/rccm.202301-0177ED
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  3. Article ; Online: Targeting Danger Signals to Rescue Fibrosis.

    Tsoyi, Konstantin / Rosas, Ivan O

    American journal of respiratory cell and molecular biology

    2022  Volume 66, Issue 5, Page(s) 468–470

    MeSH term(s) Humans ; Lung/pathology ; Lung Injury/pathology ; Pulmonary Fibrosis/pathology ; Radiation Injuries/pathology
    Language English
    Publishing date 2022-03-09
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2022-0022ED
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  4. Article ; Online: Pirfenidone in rheumatoid arthritis-associated interstitial lung disease - Authors' reply.

    Hurwitz, Shelley / Maurer, Rie / Solomon, Joshua J / Rosas, Ivan O

    The Lancet. Respiratory medicine

    2023  Volume 11, Issue 6, Page(s) e52

    MeSH term(s) Humans ; Lung Diseases, Interstitial/etiology ; Lung Diseases, Interstitial/complications ; Arthritis, Rheumatoid/complications ; Arthritis, Rheumatoid/drug therapy ; Pyridones/therapeutic use
    Chemical Substances pirfenidone (D7NLD2JX7U) ; Pyridones
    Language English
    Publishing date 2023-03-29
    Publishing country England
    Document type Letter ; Comment
    ZDB-ID 2686754-0
    ISSN 2213-2619 ; 2213-2600
    ISSN (online) 2213-2619
    ISSN 2213-2600
    DOI 10.1016/S2213-2600(23)00131-5
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  5. Article ; Online: Understanding post-COVID-19 interstitial lung disease (ILD): a new fibroinflammatory disease entity.

    Mehta, Puja / Rosas, Ivan O / Singer, Mervyn

    Intensive care medicine

    2022  Volume 48, Issue 12, Page(s) 1803–1806

    MeSH term(s) Humans ; COVID-19/complications ; Lung Diseases, Interstitial/complications ; SARS-CoV-2 ; Lung ; Retrospective Studies
    Language English
    Publishing date 2022-09-08
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80387-x
    ISSN 1432-1238 ; 0340-0964 ; 0342-4642 ; 0935-1701
    ISSN (online) 1432-1238
    ISSN 0340-0964 ; 0342-4642 ; 0935-1701
    DOI 10.1007/s00134-022-06877-w
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  6. Article ; Online: Interleukin-6 Receptor Antagonists in Critically Ill Patients with Covid-19. Reply.

    Rosas, Ivan O / Raby, Benjamin / Tsai, Larry

    The New England journal of medicine

    2021  Volume 385, Issue 12, Page(s) 1149

    Language English
    Publishing date 2021-08-18
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMc2108482
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  7. Article ; Online: Imaging and molecular biomarkers: a novel approach to screen populations at risk of pulmonary fibrosis?

    Rosas, Ivan O

    The European respiratory journal

    2016  Volume 48, Issue 5, Page(s) 1271–1273

    Language English
    Publishing date 2016-11
    Publishing country England
    Document type Editorial
    ZDB-ID 639359-7
    ISSN 1399-3003 ; 0903-1936
    ISSN (online) 1399-3003
    ISSN 0903-1936
    DOI 10.1183/13993003.01673-2016
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  8. Article: Design of the STRIVE-IPF Trial- Study of Therapeutic Plasma Exchange, Rituximab, and Intravenous Immunoglobulin for Acute Exacerbations of Idiopathic Pulmonary Fibrosis.

    Kulkarni, Tejaswini / Criner, Gerard J / Kass, Daniel J / Rosas, Ivan O / Scholand, Mary Beth / Dilling, Daniel F / Summer, Ross / Duncan, Steven R

    Research square

    2024  

    Abstract: Background: Acute exacerbations of idiopathic pulmonary fibrosis (AE-IPF) affect a significant proportion of patients with IPF. There are limited data to inform therapeutic strategies for AEIPF, despite its high mortality. We discuss the rationale and ... ...

    Abstract Background: Acute exacerbations of idiopathic pulmonary fibrosis (AE-IPF) affect a significant proportion of patients with IPF. There are limited data to inform therapeutic strategies for AEIPF, despite its high mortality. We discuss the rationale and design of STRIVE-IPF, a randomized, multi-center, open-label Phase IIb clinical trial to determine the efficacy of combined therapeutic plasma exchange (TPE), rituximab, and intravenous immunoglobulin (IVIG), in comparison to treatment as usual (TAU), among patients with acute IPF exacerbations.
    Methods: The STRIVE-IPF trial will randomize 51 patients among five sites in the United States. The inclusion criteria have been designed to select a study population with AE-IPF, as defined by American Thoracic Society criteria, while excluding patients with an alternative cause for a respiratory decompensation. The primary endpoint of this trial is six-month survival. Secondary endpoints include supplement oxygen requirement and six-minute walk distance which will be assessed immediately prior to treatment and after completion of therapy on day 19, as well as at periodic subsequent visits.
    Discussion: The experimental AE-IPF therapy proposed in this clinical trial was adapted from treatment regimens used in other antibody-mediated diseases. The regimen is initiated with TPE, which is expected to rapidly reduce circulating autoantibodies, followed by rituximab to reduce B-cells and finally IVIG, which likely has multiple effects, including affecting feedback inhibition of residual B-cells by Fc receptor occupancy. We have reported potential benefits of this experimental therapy for AE-IPF in previous anecdotal reports. This clinical trial has the potential to profoundly affect current paradigms and treatment approaches to patients with AE-IPF.Trial Registration ClinicalTrials.gov identifier: NCT03286556.
    Language English
    Publishing date 2024-02-28
    Publishing country United States
    Document type Preprint
    DOI 10.21203/rs.3.rs-3962419/v1
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  9. Article ; Online: Design of the STRIVE-IPF trial- study of therapeutic plasma exchange, rituximab, and intravenous immunoglobulin for acute exacerbations of idiopathic pulmonary fibrosis.

    Kulkarni, Tejaswini / Criner, Gerard J / Kass, Daniel J / Rosas, Ivan O / Scholand, Mary Beth / Dilling, Daniel F / Summer, Ross / Duncan, Steven R

    BMC pulmonary medicine

    2024  Volume 24, Issue 1, Page(s) 143

    Abstract: Background: Acute exacerbations of idiopathic pulmonary fibrosis (AE-IPF) affect a significant proportion of patients with IPF. There are limited data to inform therapeutic strategies for AE-IPF, despite its high mortality. We discuss the rationale and ... ...

    Abstract Background: Acute exacerbations of idiopathic pulmonary fibrosis (AE-IPF) affect a significant proportion of patients with IPF. There are limited data to inform therapeutic strategies for AE-IPF, despite its high mortality. We discuss the rationale and design of STRIVE-IPF, a randomized, multi-center, open-label Phase IIb clinical trial to determine the efficacy of combined therapeutic plasma exchange (TPE), rituximab, and intravenous immunoglobulin (IVIG), in comparison to treatment as usual (TAU), among patients with acute IPF exacerbations.
    Methods: The STRIVE-IPF trial will randomize 51 patients among five sites in the United States. The inclusion criteria have been designed to select a study population with AE-IPF, as defined by American Thoracic Society criteria, while excluding patients with an alternative cause for a respiratory decompensation. The primary endpoint of this trial is six-month survival. Secondary endpoints include supplement oxygen requirement and six-minute walk distance which will be assessed immediately prior to treatment and after completion of therapy on day 19, as well as at periodic subsequent visits.
    Discussion: The experimental AE-IPF therapy proposed in this clinical trial was adapted from treatment regimens used in other antibody-mediated diseases. The regimen is initiated with TPE, which is expected to rapidly reduce circulating autoantibodies, followed by rituximab to reduce B-cells and finally IVIG, which likely has multiple effects, including affecting feedback inhibition of residual B-cells by Fc receptor occupancy. We have reported potential benefits of this experimental therapy for AE-IPF in previous anecdotal reports. This clinical trial has the potential to profoundly affect current paradigms and treatment approaches to patients with AE-IPF.
    Trial registration: ClinicalTrials.gov identifier: NCT03286556.
    MeSH term(s) Humans ; Idiopathic Interstitial Pneumonias/complications ; Idiopathic Pulmonary Fibrosis/drug therapy ; Immunoglobulins, Intravenous/therapeutic use ; Plasma Exchange ; Rituximab/therapeutic use
    Chemical Substances Immunoglobulins, Intravenous ; Rituximab (4F4X42SYQ6)
    Language English
    Publishing date 2024-03-20
    Publishing country England
    Document type Clinical Trial, Phase II ; Journal Article ; Multicenter Study ; Randomized Controlled Trial
    ZDB-ID 2059871-3
    ISSN 1471-2466 ; 1471-2466
    ISSN (online) 1471-2466
    ISSN 1471-2466
    DOI 10.1186/s12890-024-02957-3
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  10. Article ; Online: Pathogenic Mechanisms Underlying Idiopathic Pulmonary Fibrosis.

    Moss, Benjamin J / Ryter, Stefan W / Rosas, Ivan O

    Annual review of pathology

    2021  Volume 17, Page(s) 515–546

    Abstract: The pathogenesis of idiopathic pulmonary fibrosis (IPF) involves a complex interplay of cell types and signaling pathways. Recurrent alveolar epithelial cell (AEC) injury may occur in the context of predisposing factors (e.g., genetic, environmental, ... ...

    Abstract The pathogenesis of idiopathic pulmonary fibrosis (IPF) involves a complex interplay of cell types and signaling pathways. Recurrent alveolar epithelial cell (AEC) injury may occur in the context of predisposing factors (e.g., genetic, environmental, epigenetic, immunologic, and gerontologic), leading to metabolic dysfunction, senescence, aberrant epithelial cell activation, and dysregulated epithelial repair. The dysregulated epithelial cell interacts with mesenchymal, immune, and endothelial cells via multiple signaling mechanisms to trigger fibroblast and myofibroblast activation. Recent single-cell RNA sequencing studies of IPF lungs support the epithelial injury model. These studies have uncovered a novel type of AEC with characteristics of an aberrant basal cell, which may disrupt normal epithelial repair and propagate a profibrotic phenotype. Here, we review the pathogenesis of IPF in the context of novel bioinformatics tools as strategies to discover pathways of disease, cell-specific mechanisms, and cell-cell interactions that propagate the profibrotic niche.
    MeSH term(s) Endothelial Cells/pathology ; Humans ; Idiopathic Pulmonary Fibrosis/genetics ; Idiopathic Pulmonary Fibrosis/metabolism ; Idiopathic Pulmonary Fibrosis/pathology ; Lung/metabolism ; Lung/pathology ; Signal Transduction
    Language English
    Publishing date 2021-11-23
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2227429-7
    ISSN 1553-4014 ; 1553-4006
    ISSN (online) 1553-4014
    ISSN 1553-4006
    DOI 10.1146/annurev-pathol-042320-030240
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