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Article ; Online: Mechanisms and consequences of oxidative stress in lung disease: therapeutic implications for an aging populace.

Hecker, Louise

American journal of physiology. Lung cellular and molecular physiology

2017 Volume 314, Issue 4, Page(s) L642–L653

Abstract: The rapid expansion of the elderly population has led to the recent epidemic of age-related diseases, including increased incidence and mortality of chronic and acute lung diseases. Numerous studies have implicated aging and oxidative stress in the ... ...

Abstract	The rapid expansion of the elderly population has led to the recent epidemic of age-related diseases, including increased incidence and mortality of chronic and acute lung diseases. Numerous studies have implicated aging and oxidative stress in the pathogenesis of various pulmonary diseases; however, despite recent advances in these fields, the specific contributions of aging and oxidative stress remain elusive. This review will discuss the consequences of aging on lung morphology and physiology, and how redox imbalance with aging contributes to lung disease susceptibility. Here, we focus on three lung diseases for which aging is a significant risk factor: acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD), and idiopathic pulmonary fibrosis (IPF). Preclinical and clinical development for redox- and senescence-altering therapeutic strategies are discussed, as well as scientific advancements that may direct current and future therapeutic development. A deeper understanding of how aging impacts normal lung function, redox balance, and injury-repair processes will inspire the development of new therapies to prevent and/or reverse age-associated pulmonary diseases, and ultimately increase health span and longevity. This review is intended to encourage basic, clinical, and translational research that will bridge knowledge gaps at the intersection of aging, oxidative stress, and lung disease to fuel the development of more effective therapeutic strategies for lung diseases that disproportionately afflict the elderly.
MeSH term(s)	Aging ; Animals ; Humans ; Lung Diseases/metabolism ; Lung Diseases/pathology ; Lung Diseases/therapy ; Oxidative Stress
Language	English
Publishing date	2017-12-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00275.2017
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Article ; Online: NADPH oxidases: Pathophysiology and therapeutic potential in age-associated pulmonary fibrosis.

Kato, Kosuke / Hecker, Louise

Redox biology

2020 Volume 33, Page(s) 101541

Abstract: Oxidative stress has been associated with a number of human fibrotic diseases, including idiopathic pulmonary fibrosis (IPF). Although oxidative stress is associated with both fibrosis and aging, the precise cellular sources(s) of reactive oxygen species ...

Abstract	Oxidative stress has been associated with a number of human fibrotic diseases, including idiopathic pulmonary fibrosis (IPF). Although oxidative stress is associated with both fibrosis and aging, the precise cellular sources(s) of reactive oxygen species (ROS) that contribute to the disease pathogenesis remain poorly understood. NADPH oxidase (Nox) enzymes are an evolutionarily conserved family, where their only known function is the production of ROS. A growing body of evidence supports a link between excessive Nox-derived ROS and numerous chronic diseases (including fibrotic disease), which is most prevalent among the elderly population. In this review, we examine the evidence for Nox isoforms in the pathogenesis of IPF, and the potential to target this enzyme family for the treatment of IPF and related fibrotic disorders. A better understanding of the Nox-mediated redox imbalance in aging may be critical to the development of more effective therapeutic strategies for age-associated fibrotic disorders. Strategies aimed at specifically blocking the source(s) of ROS through Nox inhibition may prove to be more effective as anti-fibrotic therapies, as compared to antioxidant approaches. This review also discusses the potential of Nox-targeting therapeutics currently in development.
MeSH term(s)	Aged ; Humans ; Idiopathic Pulmonary Fibrosis/drug therapy ; NADPH Oxidases/genetics ; NADPH Oxidases/metabolism ; Oxidation-Reduction ; Oxidative Stress ; Reactive Oxygen Species
Chemical Substances	Reactive Oxygen Species ; NADPH Oxidases (EC 1.6.3.-)
Language	English
Publishing date	2020-04-17
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2020.101541
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Article ; Online: Contracting scars from fibrin drops.

Robinson, Stephen / Parigoris, Eric / Chang, Jonathan / Hecker, Louise / Takayama, Shuichi

Integrative biology : quantitative biosciences from nano to macro

2022 Volume 14, Issue 1, Page(s) 1–12

Abstract: This paper describes a microscale fibroplasia and contraction model that is based on fibrin-embedded lung fibroblasts and provides a convenient visual readout of fibrosis. Cell-laden fibrin microgel drops are formed by aqueous two-phase microprinting. ... ...

Abstract	This paper describes a microscale fibroplasia and contraction model that is based on fibrin-embedded lung fibroblasts and provides a convenient visual readout of fibrosis. Cell-laden fibrin microgel drops are formed by aqueous two-phase microprinting. The cells deposit extracellular matrix (ECM) molecules such as collagen while fibrin is gradually degraded. Ultimately, the cells contract the collagen-rich matrix to form a compact cell-ECM spheroid. The size of the spheroid provides the visual readout of the extent of fibroplasia. Stimulation of this wound-healing model with the profibrotic cytokine TGF-β1 leads to an excessive scar formation response that manifests as increased collagen production and larger cell-ECM spheroids. Addition of drugs also shifted the scarring profile: the FDA-approved fibrosis drugs (nintedanib and pirfenidone) and a PAI-1 inhibitor (TM5275) significantly reduced cell-ECM spheroid size. Not only is the assay useful for evaluation of antifibrotic drug effects, it is relatively sensitive; one of the few in vitro fibroplasia assays that can detect pirfenidone effects at submillimolar concentrations. Although this paper focuses on lung fibrosis, the approach opens opportunities for studying a broad range of fibrotic diseases and for evaluating antifibrotic therapeutics.
MeSH term(s)	Cells, Cultured ; Cicatrix ; Collagen/metabolism ; Extracellular Matrix/metabolism ; Fibrin ; Fibroblasts/metabolism ; Fibrosis ; Humans ; Transforming Growth Factor beta1/metabolism
Chemical Substances	Transforming Growth Factor beta1 ; Fibrin (9001-31-4) ; Collagen (9007-34-5)
Language	English
Publishing date	2022-02-19
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2480063-6
ISSN	1757-9708 ; 1757-9694
ISSN (online)	1757-9708
ISSN	1757-9694
DOI	10.1093/intbio/zyac001
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Article ; Online: Aqueous two-phase deposition and fibrinolysis of fibroblast-laden fibrin micro-scaffolds.

Robinson, Stephen / Chang, Jonathan / Parigoris, Eric / Hecker, Louise / Takayama, Shuichi

Biofabrication

2021 Volume 13, Issue 3

Abstract: This paper describes printing of microscale fibroblast-laden matrices using an aqueous two-phase approach that controls thrombin-mediated enzymatic crosslinking of fibrin. Optimization of aqueous two-phase formulations enabled polymerization of ... ...

Abstract	This paper describes printing of microscale fibroblast-laden matrices using an aqueous two-phase approach that controls thrombin-mediated enzymatic crosslinking of fibrin. Optimization of aqueous two-phase formulations enabled polymerization of consistent sub-microliter volumes of cell-laden fibrin. When plasminogen was added to these micro-scaffolds, the primary normal human lung fibroblasts converted it to plasmin, triggering gradual degradation of the fibrin. Time-lapse live-cell imaging and automated image analysis provided readouts of time to degradation of 50% of the scaffold as well as maximum degradation rate. The time required for degradation decreased linearly with cell number while it increased in a dose-dependent manner upon addition of TGF-
MeSH term(s)	Fibrin ; Fibrinolysis ; Fibroblasts ; Humans ; Wound Healing
Chemical Substances	Fibrin (9001-31-4)
Language	English
Publishing date	2021-04-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2500944-8
ISSN	1758-5090 ; 1758-5082
ISSN (online)	1758-5090
ISSN	1758-5082
DOI	10.1088/1758-5090/abdb85
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Article: Getting to the core of fibrosis: targeting redox imbalance in aging.

Hecker, Louise / Thannickal, Victor J

Annals of translational medicine

2016 Volume 4, Issue 5, Page(s) 93

Language	English
Publishing date	2016-03-22
Publishing country	China
Document type	Journal Article
ZDB-ID	2893931-1
ISSN	2305-5847 ; 2305-5839
ISSN (online)	2305-5847
ISSN	2305-5839
DOI	10.21037/atm.2015.12.45
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Article: Lung-Targeted Delivery of Dimethyl Fumarate Promotes the Reversal of Age-Dependent Established Lung Fibrosis

Kato, Kosuke / Papageorgiou, Ioannis / Shin, Yoon-Joo / Kleinhenz, Jennifer M. / Palumbo, Sunny / Hahn, Seongmin / Irish, Joseph D. / Rounseville, Skye P. / Knox, Kenneth S. / Hecker, Louise

Antioxidants. 2022 Feb. 28, v. 11, no. 3

2022

Abstract: Idiopathic pulmonary fibrosis (IPF), a severe and deadly form of lung fibrosis, is widely regarded as a disease of aging. We previously demonstrated that aged mice with persistent lung fibrosis and IPF lung myofibroblasts exhibit deficient Nrf2-mediated ... ...

Abstract	Idiopathic pulmonary fibrosis (IPF), a severe and deadly form of lung fibrosis, is widely regarded as a disease of aging. We previously demonstrated that aged mice with persistent lung fibrosis and IPF lung myofibroblasts exhibit deficient Nrf2-mediated antioxidant responses. Tecfidera is an orally administered FDA-approved drug for the treatment of multiple sclerosis, where the active pharmaceutical ingredient is dimethyl fumarate (DMF), an active Nrf2 activator. However, no studies have evaluated the efficacy of DMF for age-associated persistent lung fibrosis. Here, we demonstrate that in IPF lung fibroblasts, DMF treatment inhibited both TGF-β-mediated pro-fibrotic phenotypes and led to a reversal of established pro-fibrotic phenotypes. We also evaluated the pre-clinical efficacy of lung-targeted (inhaled) vs. systemic (oral) delivery of DMF in an aging murine model of bleomycin-induced persistent lung fibrosis. DMF or vehicle was administered daily to aged mice by oral gavage or intranasal delivery from 3–6 weeks post-injury when mice exhibited non-resolving lung fibrosis. In contrast to systemic (oral) delivery, only lung-targeted (inhaled) delivery of DMF restored lung Nrf2 expression levels, reduced lung oxidative stress, and promoted the resolution of age-dependent established fibrosis. This is the first study to demonstrate the efficacy of lung-targeted DMF delivery to promote the resolution of age-dependent established lung fibrosis.
Keywords	active pharmaceutical ingredients ; animal models ; antioxidants ; dimethyl fumarate ; drugs ; fibroblasts ; fibrosis ; lungs ; oxidative stress ; pulmonary fibrosis ; sclerosis
Language	English
Dates of publication	2022-0228
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox11030492
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Active transcription in the vascular bed characterizes rapid progression in idiopathic pulmonary fibrosis.

Sharma, Nirmal S / Patel, Kapil / Sari, Ezgi / Shankar, Shruti / Gastanadui, Maria G / Moncada-Giraldo, Diego / Soto-Vazquez, Yixel / Stacks, Delores / Hecker, Louise / Dsouza, Kevin / Banday, Mudassir / O'Neill, Edward / Benson, Paul / Payne, Gregory / Margaroli, Camilla / Gaggar, Amit

The Journal of clinical investigation

2023 Volume 133, Issue 16

MeSH term(s)	Humans ; Idiopathic Pulmonary Fibrosis/genetics ; Disease Progression ; Lung
Language	English
Publishing date	2023-08-15
Publishing country	United States
Document type	Research Support, N.I.H., Extramural ; Letter ; Research Support, U.S. Gov't, Non-P.H.S. ; 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/JCI165976
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Article: Lung-Targeted Delivery of Dimethyl Fumarate Promotes the Reversal of Age-Dependent Established Lung Fibrosis.

Kato, Kosuke / Papageorgiou, Ioannis / Shin, Yoon-Joo / Kleinhenz, Jennifer M / Palumbo, Sunny / Hahn, Seongmin / Irish, Joseph D / Rounseville, Skye P / Knox, Kenneth S / Hecker, Louise

Antioxidants (Basel, Switzerland)

2022 Volume 11, Issue 3

Abstract	Idiopathic pulmonary fibrosis (IPF), a severe and deadly form of lung fibrosis, is widely regarded as a disease of aging. We previously demonstrated that aged mice with persistent lung fibrosis and IPF lung myofibroblasts exhibit deficient Nrf2-mediated antioxidant responses. Tecfidera is an orally administered FDA-approved drug for the treatment of multiple sclerosis, where the active pharmaceutical ingredient is dimethyl fumarate (DMF), an active Nrf2 activator. However, no studies have evaluated the efficacy of DMF for age-associated persistent lung fibrosis. Here, we demonstrate that in IPF lung fibroblasts, DMF treatment inhibited both TGF-β-mediated pro-fibrotic phenotypes and led to a reversal of established pro-fibrotic phenotypes. We also evaluated the pre-clinical efficacy of lung-targeted (inhaled) vs. systemic (oral) delivery of DMF in an aging murine model of bleomycin-induced persistent lung fibrosis. DMF or vehicle was administered daily to aged mice by oral gavage or intranasal delivery from 3-6 weeks post-injury when mice exhibited non-resolving lung fibrosis. In contrast to systemic (oral) delivery, only lung-targeted (inhaled) delivery of DMF restored lung Nrf2 expression levels, reduced lung oxidative stress, and promoted the resolution of age-dependent established fibrosis. This is the first study to demonstrate the efficacy of lung-targeted DMF delivery to promote the resolution of age-dependent established lung fibrosis.
Language	English
Publishing date	2022-02-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox11030492
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Article ; Online: Nonresolving fibrotic disorders: idiopathic pulmonary fibrosis as a paradigm of impaired tissue regeneration.

Hecker, Louise / Thannickal, Victor J

The American journal of the medical sciences

2011 Volume 341, Issue 6, Page(s) 431–434

Abstract: The pathogenesis idiopathic pulmonary of fibrosis and related fibrosis lung disorders are complex and poorly understood. This likely involves cellular mechanisms that result in loss of cellular homeostasis leading to aberrant alveolar wall remodeling ... ...

Abstract	The pathogenesis idiopathic pulmonary of fibrosis and related fibrosis lung disorders are complex and poorly understood. This likely involves cellular mechanisms that result in loss of cellular homeostasis leading to aberrant alveolar wall remodeling through the excessive deposition of connective tissue matrices. Impaired tissue regeneration and dysregulation of cell death in lung fibroblasts and epithelial cells appear to be important in the initiation and progression of these disorders. This review summarizes current understanding in this area to stimulate research into the development of novel therapeutic strategies that prevent, halt or reverse the progression of lung fibrosis.
MeSH term(s)	Apoptosis ; Epithelial Cells/pathology ; Fibroblasts/pathology ; Fibrosis/pathology ; Fibrosis/physiopathology ; Humans ; Idiopathic Pulmonary Fibrosis/pathology ; Idiopathic Pulmonary Fibrosis/physiopathology ; Lung/pathology ; Lung/physiopathology ; Regeneration
Language	English
Publishing date	2011-08-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	82078-7
ISSN	1538-2990 ; 0002-9629
ISSN (online)	1538-2990
ISSN	0002-9629
DOI	10.1097/MAJ.0b013e31821a9d66
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Article ; Online: MUC1 contributes to goblet cell metaplasia and MUC5AC expression in response to cigarette smoke in vivo.

Kato, Kosuke / Chang, Eugene H / Chen, Yin / Lu, Wenju / Kim, Marianne M / Niihori, Maki / Hecker, Louise / Kim, Kwang Chul

American journal of physiology. Lung cellular and molecular physiology

2020 Volume 319, Issue 1, Page(s) L82–L90

Abstract: Goblet cell metaplasia (GCM) and mucin overproduction are a hallmark of chronic rhinosinusitis (CRS) and chronic obstructive pulmonary disease (COPD). In the airways, cigarette smoke (CS) induces activation of the epidermal growth factor receptor (EGFR) ... ...

Abstract	Goblet cell metaplasia (GCM) and mucin overproduction are a hallmark of chronic rhinosinusitis (CRS) and chronic obstructive pulmonary disease (COPD). In the airways, cigarette smoke (CS) induces activation of the epidermal growth factor receptor (EGFR) leading to GCM and overexpression of the gel-forming mucin MUC5AC. Although previous studies have demonstrated that a membrane-bound mucin, MUC1, modulates the activation of CS-induced EGFR, the role of MUC1 in CS-induced GCM and mucin overproduction has not been explored. In response to CS exposure, wild-type (WT) rats displayed Muc1 translocation from the apical surface of airway epithelium to the intracellular compartment of hyperplastic intermediate cells, EGFR phosphorylation, GCM, and Muc5ac overproduction. Similarly, human CRS sinonasal tissues demonstrated hyperplasia of intermediate cells enriched with MUC1 in the intracellular compartment, which was accompanied by GCM and increased MUC5AC expression. To further evaluate the role of Muc1 in vivo, a Muc1 knockout (KO) rat (MUC in humans and Muc in animals) was developed. In contrast to WT littermates, Muc1-KO rats exhibited no activation of EGFR, and were protected from GCM and Muc5ac overproduction. Genetic knockdown of MUC1 in human lung or Muc1 knockout in primary rat airway epithelial cells led to significantly diminished EGF-induced MUC5AC production. Together, these findings suggest that MUC1-dependent EGFR activation mediates CS-induced GCM and mucin overproduction. Strategies designed to suppress MUC1-dependent EGFR activation may provide a novel therapeutic approach for treating mucin hypersecretion in CRS and COPD.
MeSH term(s)	Animals ; Cell Line, Tumor ; Cell Polarity ; Epithelial Cells/metabolism ; Epithelium/metabolism ; Epithelium/pathology ; ErbB Receptors/metabolism ; Goblet Cells/metabolism ; Goblet Cells/pathology ; Metaplasia ; Mucin 5AC/metabolism ; Mucin-1/metabolism ; Phosphorylation ; Rats, Sprague-Dawley ; Smoking/adverse effects
Chemical Substances	Mucin 5AC ; Mucin-1 ; ErbB Receptors (EC 2.7.10.1)
Language	English
Publishing date	2020-05-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00049.2019
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Uc I Zs.89: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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