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  1. Article ; Online: Demystifying the Enigmatic Fibroblast in Pulmonary Fibrosis.

    Zhou, Yong / Thannickal, Victor J

    American journal of respiratory cell and molecular biology

    2023  Volume 69, Issue 1, Page(s) 1–2

    MeSH term(s) Humans ; Pulmonary Fibrosis/pathology ; Fibroblasts/pathology ; Lung/pathology
    Language English
    Publishing date 2023-04-11
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Comment
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2023-0090ED
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Myofibroblast Functions in Tissue Repair and Fibrosis: An Introduction.

    Thannickal, Victor J

    Methods in molecular biology (Clifton, N.J.)

    2021  Volume 2299, Page(s) 9–15

    Abstract: Our understanding of myofibroblast biology has advanced over the past two decades, and the seemingly antagonistic roles of these cells in both normal tissue repair and fibrotic diseases are better reconciled. An age-related loss of cellular plasticity ... ...

    Abstract Our understanding of myofibroblast biology has advanced over the past two decades, and the seemingly antagonistic roles of these cells in both normal tissue repair and fibrotic diseases are better reconciled. An age-related loss of cellular plasticity that results in impaired capacity for de-differentiation and apoptosis susceptibility may predispose individuals to non-resolving and progressive fibrotic disorders involving diverse organ systems.
    MeSH term(s) Aging/physiology ; Animals ; Apoptosis ; Cell Dedifferentiation ; Extracellular Matrix/physiology ; Fibrosis/physiopathology ; Humans ; Myofibroblasts/physiology ; Wound Healing
    Language English
    Publishing date 2021-05-24
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-1382-5_2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Autophagy in Idiopathic Pulmonary Fibrosis: Predisposition of the Aging Lung to Fibrosis?

    Zmijewski, Jaroslaw W / Thannickal, Victor J

    American journal of respiratory cell and molecular biology

    2023  Volume 68, Issue 1, Page(s) 3–4

    MeSH term(s) Humans ; Idiopathic Pulmonary Fibrosis/genetics ; Lung ; Aging ; Autophagy ; Ubiquitin-Specific Proteases
    Chemical Substances USP13 protein, human (EC 3.4.19.12) ; Ubiquitin-Specific Proteases (EC 3.4.19.12)
    Language English
    Publishing date 2023-02-10
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Comment
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2022-0379ED
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Redox biology and therapeutics in chronic lung disease.

    Thannickal, Victor J

    Redox biology

    2020  Volume 33, Page(s) 101579

    MeSH term(s) Biology ; Humans ; Lung Diseases/drug therapy ; Oxidation-Reduction ; Oxidative Stress
    Language English
    Publishing date 2020-05-11
    Publishing country Netherlands
    Document type Editorial ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2701011-9
    ISSN 2213-2317 ; 2213-2317
    ISSN (online) 2213-2317
    ISSN 2213-2317
    DOI 10.1016/j.redox.2020.101579
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Elixir of Youth: Lipid Signaling Chaperones Synthesized in the Liver.

    Thannickal, Victor J

    Developmental cell

    2020  Volume 53, Issue 6, Page(s) 625–626

    Abstract: Organ fibrosis represents a default tissue program activated when regenerative capacity is limited. In this issue of Developmental Cell, Ding et al. identify a lipid signaling pathway involving the liver synthesized chaperone ApoM as a circulating pro- ... ...

    Abstract Organ fibrosis represents a default tissue program activated when regenerative capacity is limited. In this issue of Developmental Cell, Ding et al. identify a lipid signaling pathway involving the liver synthesized chaperone ApoM as a circulating pro-regenerative mediator that is deficient in aging and mitigates fibrosis in distant organs.
    MeSH term(s) Liver ; Lysophospholipids ; Signal Transduction ; Sphingosine/analogs & derivatives
    Chemical Substances Lysophospholipids ; sphingosine 1-phosphate (26993-30-6) ; Sphingosine (NGZ37HRE42)
    Language English
    Publishing date 2020-06-20
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2054967-2
    ISSN 1878-1551 ; 1534-5807
    ISSN (online) 1878-1551
    ISSN 1534-5807
    DOI 10.1016/j.devcel.2020.06.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: ENERGY SENSING PATHWAYS IN AGING AND CHRONIC LUNG DISEASE.

    Thannickal, Victor J

    Transactions of the American Clinical and Climatological Association

    2020  Volume 131, Page(s) 286–293

    Abstract: Aging is associated with an increased risk of a number of clinical syndromes, including chronic lung disease. There have been significant advances in our understanding of the biology of aging leading to the elucidation of the so-called "hallmarks of ... ...

    Abstract Aging is associated with an increased risk of a number of clinical syndromes, including chronic lung disease. There have been significant advances in our understanding of the biology of aging leading to the elucidation of the so-called "hallmarks of aging." The cause-effect relationships between various hallmarks such as dysregulated nutrient sensing, mitochondrial dysfunction, and cellular senescence are not well understood. Here, I discuss the evidence for alterations in energy/metabolic sensing pathways in the degenerative chronic lung disease called idiopathic pulmonary fibrosis (IPF). The pathobiological mechanisms by which this defect may contribute to age-related susceptibility to IPF and potentially other diseases of the elderly are also discussed.
    Language English
    Publishing date 2020-07-13
    Publishing country United States
    Document type Journal Article
    ZDB-ID 603823-2
    ISSN 0065-7778
    ISSN 0065-7778
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: NOTCH-ing up Surface Tension in the Fibrotic Lung.

    Lasky, Joseph A / Thannickal, Victor J

    American journal of respiratory and critical care medicine

    2022  Volume 207, Issue 3, Page(s) 235–236

    MeSH term(s) Humans ; Pulmonary Fibrosis ; Surface-Active Agents ; Surface Tension ; Pulmonary Surfactants ; Lung/diagnostic imaging ; Receptor, Notch1
    Chemical Substances Surface-Active Agents ; Pulmonary Surfactants ; NOTCH1 protein, human ; Receptor, Notch1
    Language English
    Publishing date 2022-11-09
    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.202210-1901ED
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: The lung mesenchyme in development, regeneration, and fibrosis.

    El Agha, Elie / Thannickal, Victor J

    The Journal of clinical investigation

    2023  Volume 133, Issue 14

    Abstract: Mesenchymal cells are uniquely located at the interface between the epithelial lining and the stroma, allowing them to act as a signaling hub among diverse cellular compartments of the lung. During embryonic and postnatal lung development, mesenchyme- ... ...

    Abstract Mesenchymal cells are uniquely located at the interface between the epithelial lining and the stroma, allowing them to act as a signaling hub among diverse cellular compartments of the lung. During embryonic and postnatal lung development, mesenchyme-derived signals instruct epithelial budding, branching morphogenesis, and subsequent structural and functional maturation. Later during adult life, the mesenchyme plays divergent roles wherein its balanced activation promotes epithelial repair after injury while its aberrant activation can lead to pathological remodeling and fibrosis that are associated with multiple chronic pulmonary diseases, including bronchopulmonary dysplasia, idiopathic pulmonary fibrosis, and chronic obstructive pulmonary disease. In this Review, we discuss the involvement of the lung mesenchyme in various morphogenic, neomorphogenic, and dysmorphogenic aspects of lung biology and health, with special emphasis on lung fibroblast subsets and smooth muscle cells, intercellular communication, and intrinsic mesenchymal mechanisms that drive such physiological and pathophysiological events throughout development, homeostasis, injury repair, regeneration, and aging.
    MeSH term(s) Infant, Newborn ; Humans ; Lung/pathology ; Pulmonary Disease, Chronic Obstructive/pathology ; Fibrosis ; Regeneration ; Mesoderm/pathology ; Epithelial Cells/pathology
    Language English
    Publishing date 2023-07-17
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI170498
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Redox biology and therapeutics in chronic lung disease

    Victor J. Thannickal

    Redox Biology, Vol 33, Iss , Pp - (2020)

    2020  

    Keywords Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2020-06-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  10. Article ; Online: Pre-clinical evidence of a dual NADPH oxidase 1/4 inhibitor (setanaxib) in liver, kidney and lung fibrosis.

    Thannickal, Victor J / Jandeleit-Dahm, Karin / Szyndralewiez, Cédric / Török, Natalie J

    Journal of cellular and molecular medicine

    2023  Volume 27, Issue 4, Page(s) 471–481

    Abstract: Fibrosis describes a dysregulated tissue remodelling response to persistent cellular injury and is the final pathological consequence of many chronic diseases that affect the liver, kidney and lung. Nicotinamide adenine dinucleotide phosphate (NADPH)- ... ...

    Abstract Fibrosis describes a dysregulated tissue remodelling response to persistent cellular injury and is the final pathological consequence of many chronic diseases that affect the liver, kidney and lung. Nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase (NOX) enzymes produce reactive oxygen species (ROS) as their primary function. ROS derived from NOX1 and NOX4 are key mediators of liver, kidney and lung fibrosis. Setanaxib (GKT137831) is a first-in-class, dual inhibitor of NOX1/4 and is the first NOX inhibitor to progress to clinical trial investigation. The anti-fibrotic effects of setanaxib in liver, kidney and lung fibrosis are supported by multiple lines of pre-clinical evidence. However, despite advances in our understanding, the precise roles of NOX1/4 in fibrosis require further investigation. Additionally, there is a translational gap between the pre-clinical observations of setanaxib to date and the applicability of these to human patients within a clinical setting. This narrative review critically examines the role of NOX1/4 in liver, kidney and lung fibrosis, alongside the available evidence investigating setanaxib as a therapeutic agent in pre-clinical models of disease. We discuss the potential clinical translatability of this pre-clinical evidence, which provides rationale to explore NOX1/4 inhibition by setanaxib across various fibrotic pathologies in clinical trials involving human patients.
    MeSH term(s) Humans ; NADPH Oxidase 1 ; Reactive Oxygen Species ; Pulmonary Fibrosis/pathology ; Hepatic Stellate Cells ; Liver/pathology ; NADPH Oxidases ; Kidney/pathology ; NADPH Oxidase 4
    Chemical Substances setanaxib (45II35329V) ; NADPH Oxidase 1 (EC 1.6.3.-) ; Reactive Oxygen Species ; NADPH Oxidases (EC 1.6.3.-) ; NADPH Oxidase 4 (EC 1.6.3.-)
    Language English
    Publishing date 2023-01-19
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2074559-X
    ISSN 1582-4934 ; 1582-4934 ; 1582-1838
    ISSN (online) 1582-4934
    ISSN 1582-4934 ; 1582-1838
    DOI 10.1111/jcmm.17649
    Database MEDical Literature Analysis and Retrieval System OnLINE

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