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  1. Article ; Online: Idiopathic Pulmonary Fibrosis: From Common Microscopy to Single-Cell Biology and Precision Medicine.

    Selman, Moisés / Pardo, Annie

    American journal of respiratory and critical care medicine

    2024  Volume 209, Issue 9, Page(s) 1074–1081

    MeSH term(s) Humans ; Idiopathic Pulmonary Fibrosis/physiopathology ; Precision Medicine/methods ; Single-Cell Analysis/methods ; Microscopy/methods
    Language English
    Publishing date 2024-01-29
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 1180953-x
    ISSN 1535-4970 ; 0003-0805 ; 1073-449X
    ISSN (online) 1535-4970
    ISSN 0003-0805 ; 1073-449X
    DOI 10.1164/rccm.202309-1573PP
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Diagnostic unification of usual interstitial pneumonia is a step back - Authors' reply.

    Selman, Moisés / Pardo, Annie / Wells, Athol U

    The Lancet. Respiratory medicine

    2023  Volume 11, Issue 6, Page(s) e54

    MeSH term(s) Humans ; Idiopathic Pulmonary Fibrosis/diagnosis ; Lung
    Language English
    Publishing date 2023-04-07
    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)00127-3
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  3. Article ; Online: Usual interstitial pneumonia as a stand-alone diagnostic entity: the case for a paradigm shift?

    Selman, Moisés / Pardo, Annie / Wells, Athol U

    The Lancet. Respiratory medicine

    2023  Volume 11, Issue 2, Page(s) 188–196

    Abstract: Usual interstitial pneumonia (UIP) is characterised by a distinctive morphological and radiological appearance that was considered the pathognomonic hallmark of idiopathic pulmonary fibrosis (IPF). However, this peculiar lung remodelling pattern is also ... ...

    Abstract Usual interstitial pneumonia (UIP) is characterised by a distinctive morphological and radiological appearance that was considered the pathognomonic hallmark of idiopathic pulmonary fibrosis (IPF). However, this peculiar lung remodelling pattern is also seen in other fibrotic interstitial lung diseases, including hypersensitivity pneumonitis, and connective tissue diseases. In this Personal View, we advocate the designation of a UIP pattern as a single, discrete diagnostic entity, amalgamating its primary form and secondary processes in disorders such as hypersensitivity pneumonitis (hypersensitivity pneumonitis with UIP), rheumatoid arthritis (rheumatoid arthritis with UIP), and others. The current separation between primary and secondary UIP is in keeping with the view that every individual interstitial lung disease must be viewed as a separate entity but does not reflect striking similarities between primary and secondary UIP in the morphological or radiological appearance, clinical behaviour, pathogenic pathways, and the efficacy of anti-fibrotic therapy. We believe that the unification of UIP as a single diagnostic entity has undeniable advantages.
    MeSH term(s) Humans ; Tomography, X-Ray Computed ; Idiopathic Pulmonary Fibrosis/diagnostic imaging ; Idiopathic Pulmonary Fibrosis/complications ; Lung Diseases, Interstitial/diagnostic imaging ; Lung Diseases, Interstitial/complications ; Lung/diagnostic imaging ; Lung/pathology ; Alveolitis, Extrinsic Allergic/diagnostic imaging ; Arthritis, Rheumatoid/complications ; Retrospective Studies
    Language English
    Publishing date 2023-01-11
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2686754-0
    ISSN 2213-2619 ; 2213-2600
    ISSN (online) 2213-2619
    ISSN 2213-2600
    DOI 10.1016/S2213-2600(22)00475-1
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  4. Article ; Online: When things go wrong: exploring possible mechanisms driving the progressive fibrosis phenotype in interstitial lung diseases.

    Selman, Moisés / Pardo, Annie

    The European respiratory journal

    2021  Volume 58, Issue 3

    Abstract: Interstitial lung diseases (ILDs) comprise a large and heterogeneous group of disorders of known and unknown aetiology characterised by diffuse damage of the lung parenchyma. In recent years it has become evident that patients with different types of ILD ...

    Abstract Interstitial lung diseases (ILDs) comprise a large and heterogeneous group of disorders of known and unknown aetiology characterised by diffuse damage of the lung parenchyma. In recent years it has become evident that patients with different types of ILD are at risk of developing progressive pulmonary fibrosis, known as progressive fibrosing ILD (PF-ILD). This is a phenotype that behaves similar to idiopathic pulmonary fibrosis, the archetypical example of progressive fibrosis. PF-ILD is not a distinct clinical entity but describes a group of ILDs with similar clinical behaviour. This phenotype may occur in diseases displaying distinct aetiologies and different biopathology during their initiation and development. Importantly, these entities may have the potential for improvement or stabilisation prior to entering the progressive fibrosing phase. The crucial questions are: 1) why does a subset of patients develop a progressive and irreversible fibrotic phenotype even with appropriate treatment? and 2) what are the possible pathogenic mechanisms driving progression? Here, we provide a framework highlighting putative mechanisms underlying progression, including genetic susceptibility, ageing, epigenetics, structural fibrotic distortion, aberrant composition and stiffness of the extracellular matrix, and the emergence of distinct pro-fibrotic cell subsets. Understanding the cellular and molecular mechanisms behind PF-ILD will provide the basis for identifying risk factors and appropriate therapeutic strategies.
    MeSH term(s) Disease Progression ; Fibrosis ; Humans ; Idiopathic Pulmonary Fibrosis/genetics ; Lung Diseases, Interstitial/genetics ; Phenotype
    Language English
    Publishing date 2021-09-09
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 639359-7
    ISSN 1399-3003 ; 0903-1936
    ISSN (online) 1399-3003
    ISSN 0903-1936
    DOI 10.1183/13993003.04507-2020
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  5. Article ; Online: From pulmonary fibrosis to progressive pulmonary fibrosis: a lethal pathobiological jump.

    Selman, Moisés / Pardo, Annie

    American journal of physiology. Lung cellular and molecular physiology

    2021  Volume 321, Issue 3, Page(s) L600–L607

    Abstract: The month of September is Pulmonary Fibrosis Awareness Month. In this context, we would like to highlight the concept of progressive pulmonary fibrosis, a common denominator/phenotype of many interstitial lung diseases other than idiopathic pulmonary ... ...

    Abstract The month of September is Pulmonary Fibrosis Awareness Month. In this context, we would like to highlight the concept of progressive pulmonary fibrosis, a common denominator/phenotype of many interstitial lung diseases other than idiopathic pulmonary fibrosis, leading to clinical deterioration, decreased quality of life, and high mortality.
    MeSH term(s) Humans ; Idiopathic Pulmonary Fibrosis ; Lung Diseases, Interstitial ; Phenotype ; Quality of Life
    Language English
    Publishing date 2021-07-28
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 1013184-x
    ISSN 1522-1504 ; 1040-0605
    ISSN (online) 1522-1504
    ISSN 1040-0605
    DOI 10.1152/ajplung.00310.2021
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  6. Article ; Online: Fibroageing: An ageing pathological feature driven by dysregulated extracellular matrix-cell mechanobiology.

    Selman, Moisés / Pardo, Annie

    Ageing research reviews

    2021  Volume 70, Page(s) 101393

    Abstract: Ageing is a multifactorial biological process leading to a progressive decline of physiological functions. The process of ageing includes numerous changes in the cells and the interactions between cell-cell and cell-microenvironment remaining as a ... ...

    Abstract Ageing is a multifactorial biological process leading to a progressive decline of physiological functions. The process of ageing includes numerous changes in the cells and the interactions between cell-cell and cell-microenvironment remaining as a critical risk factor for the development of chronic degenerative diseases. Systemic inflammation, known as inflammageing, increases as a consequence of ageing contributing to age-related morbidities. But also, persistent and uncontrolled activation of fibrotic pathways, with excessive accumulation of extracellular matrix (ECM) and organ dysfunction is markedly more frequent in the elderly. In this context, we introduce here the concept of Fibroageing, that is, the propensity to develop tissue fibrosis associated with ageing, and propose that ECM is a key player underlying this process. During ageing, molecules of the ECM become damaged through many modifications including glycation, crosslinking, and accumulation, leading to matrix stiffness which intensifies ageing-associated alterations. We provide a framework with some mechanistic hypotheses proposing that stiff ECM, in addition to the well-known activation of fibrotic positive feedback loops, affect several of the hallmarks of ageing, such as cell senescence and mitochondrial dysfunction, and in this context, is a key mechanism and a driver thread of Fibroageing.
    MeSH term(s) Aged ; Aging ; Biophysics ; Cellular Senescence ; Extracellular Matrix/pathology ; Fibrosis ; Humans
    Language English
    Publishing date 2021-06-15
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2075672-0
    ISSN 1872-9649 ; 1568-1637
    ISSN (online) 1872-9649
    ISSN 1568-1637
    DOI 10.1016/j.arr.2021.101393
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  7. Article ; Online: Pulmonary Fibrosis in the Time of COVID-19.

    Buendia-Roldan, Ivette / Valenzuela, Claudia / Selman, Moisés

    Archivos de bronconeumologia

    2022  Volume 58 Suppl 1, Page(s) 6–7

    MeSH term(s) COVID-19/complications ; Humans ; Lung/pathology ; Pulmonary Fibrosis/etiology ; Pulmonary Fibrosis/pathology ; Tomography, X-Ray Computed
    Language Spanish
    Publishing date 2022-04-15
    Publishing country Spain
    Document type Editorial
    ZDB-ID 733126-5
    ISSN 1579-2129 ; 0300-2896
    ISSN (online) 1579-2129
    ISSN 0300-2896
    DOI 10.1016/j.arbres.2022.03.007
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  8. Article ; Online: One Molecule, Two Opposite Biological Effects: The Many Faces of Matrix Metalloproteases in the Pathogenesis of Idiopathic Pulmonary Fibrosis.

    Pardo, Annie / Selman, Moises

    American journal of respiratory and critical care medicine

    2020  Volume 203, Issue 4, Page(s) 406–408

    MeSH term(s) Humans ; Idiopathic Pulmonary Fibrosis ; Matrix Metalloproteinase 9 ; Matrix Metalloproteinases
    Chemical Substances Matrix Metalloproteinases (EC 3.4.24.-) ; Matrix Metalloproteinase 9 (EC 3.4.24.35)
    Language English
    Publishing date 2020-11-21
    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.202008-3330ED
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  9. Article ; Online: The Interplay of the Genetic Architecture, Aging, and Environmental Factors in the Pathogenesis of Idiopathic Pulmonary Fibrosis.

    Pardo, Annie / Selman, Moisés

    American journal of respiratory cell and molecular biology

    2020  Volume 64, Issue 2, Page(s) 163–172

    Abstract: Idiopathic pulmonary fibrosis (IPF) is a chronic fibrosing lung disease of indeterminate etiology and limited therapeutic options. The initiation, development, and progression of IPF are influenced by genetic predisposition, aging, and host and ... ...

    Abstract Idiopathic pulmonary fibrosis (IPF) is a chronic fibrosing lung disease of indeterminate etiology and limited therapeutic options. The initiation, development, and progression of IPF are influenced by genetic predisposition, aging, and host and environmental factors, but the magnitude of the contribution of each of them and the sequence of the pathogenic events are uncertain. Current evidence indicates that accumulated environmental exposures in a genetically predisposed individual, usually over 60 years of age, leads to phenotypic and functional alterations of the lung epithelium. Aberrant activation of epithelial cells results, through a complex release of numerous mediators, in the local expansion of peculiar subsets of aggressive fibroblasts and myofibroblasts, which are crucial effector cells of fibrotic remodeling and loss of the normal lung architecture and function. Progressive increase of the mechanical stiffness activates cell-autonomous and matrix-dependent processes contributing to the perpetuation of the fibrotic response. This Perspective provides an integral overview of the major risk factors underpinning the pathogenesis of IPF, including gene variants, aging alterations, environmental factors, host risk factors, and epigenetic reprogramming.
    MeSH term(s) Aging/genetics ; Aging/pathology ; Disease Progression ; Epigenesis, Genetic/genetics ; Epithelial Cells/pathology ; Epithelium/pathology ; Fibroblasts/pathology ; Humans ; Idiopathic Pulmonary Fibrosis/genetics ; Idiopathic Pulmonary Fibrosis/pathology ; Lung/pathology ; Myofibroblasts/pathology ; Risk Factors
    Language English
    Publishing date 2020-10-05
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2020-0373PS
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  10. Article: PREFACE.

    Pérez-Padilla, Rogelio / Selman, Moisés

    Revista de investigacion clinica; organo del Hospital de Enfermedades de la Nutricion

    2019  Volume 71, Issue 1, Page(s) 5–6

    MeSH term(s) Humans ; Pulmonary Disease, Chronic Obstructive/etiology ; Pulmonary Disease, Chronic Obstructive/physiopathology ; Smoking/adverse effects ; Smoking/epidemiology
    Language English
    Publishing date 2019-02-27
    Publishing country Mexico
    Document type Introductory Journal Article
    ZDB-ID 138348-6
    ISSN 0034-8376
    ISSN 0034-8376
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