Publication

Dynamic Reciprocity: The Role of the Extracellular Matrix Microenvironment in Amplifying and Sustaining Pathological Lung Fibrosis

Burgess, J., Muizer, K., Brandsma, C. & Heijink, H., 2019, Fibrosis in Disease: An Organ-Based Guide to Disease Pathophysiology and Therapeutic Considerations. Willis, M., Yates, C. C. & Schisler, J. C. (eds.). 1 ed. Humana Press, p. 239-270 32 p. (Molecular and Translational Medicine).

Research output: Chapter in Book/Report/Conference proceedingChapterAcademicpeer-review

APA

Burgess, J., Muizer, K., Brandsma, C., & Heijink, H. (2019). Dynamic Reciprocity: The Role of the Extracellular Matrix Microenvironment in Amplifying and Sustaining Pathological Lung Fibrosis. In M. Willis, C. C. Yates, & J. C. Schisler (Eds.), Fibrosis in Disease: An Organ-Based Guide to Disease Pathophysiology and Therapeutic Considerations (1 ed., pp. 239-270). (Molecular and Translational Medicine). Humana Press. https://doi.org/10.1007/978-3-319-98143-7_9

Author

Burgess, Janette ; Muizer, Kirsten ; Brandsma, C. ; Heijink, Hilde. / Dynamic Reciprocity : The Role of the Extracellular Matrix Microenvironment in Amplifying and Sustaining Pathological Lung Fibrosis. Fibrosis in Disease: An Organ-Based Guide to Disease Pathophysiology and Therapeutic Considerations. editor / Monte Willis ; Cecelia C. Yates ; Jonathan C. Schisler. 1. ed. Humana Press, 2019. pp. 239-270 (Molecular and Translational Medicine).

Harvard

Burgess, J, Muizer, K, Brandsma, C & Heijink, H 2019, Dynamic Reciprocity: The Role of the Extracellular Matrix Microenvironment in Amplifying and Sustaining Pathological Lung Fibrosis. in M Willis, CC Yates & JC Schisler (eds), Fibrosis in Disease: An Organ-Based Guide to Disease Pathophysiology and Therapeutic Considerations. 1 edn, Molecular and Translational Medicine, Humana Press, pp. 239-270. https://doi.org/10.1007/978-3-319-98143-7_9

Standard

Dynamic Reciprocity : The Role of the Extracellular Matrix Microenvironment in Amplifying and Sustaining Pathological Lung Fibrosis. / Burgess, Janette; Muizer, Kirsten; Brandsma, C.; Heijink, Hilde.

Fibrosis in Disease: An Organ-Based Guide to Disease Pathophysiology and Therapeutic Considerations. ed. / Monte Willis; Cecelia C. Yates; Jonathan C. Schisler. 1. ed. Humana Press, 2019. p. 239-270 (Molecular and Translational Medicine).

Research output: Chapter in Book/Report/Conference proceedingChapterAcademicpeer-review

Vancouver

Burgess J, Muizer K, Brandsma C, Heijink H. Dynamic Reciprocity: The Role of the Extracellular Matrix Microenvironment in Amplifying and Sustaining Pathological Lung Fibrosis. In Willis M, Yates CC, Schisler JC, editors, Fibrosis in Disease: An Organ-Based Guide to Disease Pathophysiology and Therapeutic Considerations. 1 ed. Humana Press. 2019. p. 239-270. (Molecular and Translational Medicine). https://doi.org/10.1007/978-3-319-98143-7_9


BibTeX

@inbook{cdce4a986e9f4252929a43c593f1bc86,
title = "Dynamic Reciprocity: The Role of the Extracellular Matrix Microenvironment in Amplifying and Sustaining Pathological Lung Fibrosis",
abstract = "When taken together fibrotic lung diseases are the leading cause of mortality worldwide, but our understanding of the underlying mechanisms driving these processes is limited. The lung consists of defined parts including the airways and parenchyma. The principal building blocks of these parts are the extracellular matrix (ECM). The ECM supports cells structurally while also acting as a bioactive environment directing cellular responses during pathological events in the lung. Airway and parenchymal tissue ECM alterations characterize the changes identified in many fibrotic lung diseases, including in asthma, chronic obstructive pulmonary disease (COPD), and idiopathic pulmonary fibrosis (IPF). Characterization of the profiles of changes and investigation into how these ECM changes contribute to the disease process has been the recent focus within the field. Studies suggest that the changes in the composition, organization, and stiffness of the ECM environment in the lung may drive functional responses of cells and thereby contribute to the pathological outcome. This chapter aims to summarize the state of the art regarding the dynamic interchange of the ECM in pulmonary fibrotic diseases and the approaches for modulating these aberrations in the future. The overarching goal is to expand knowledge of the contributions of the ECM to enable a better understanding of fibrotic lung diseases and to identify novel approaches for therapeutic targeting in this area.",
author = "Janette Burgess and Kirsten Muizer and C. Brandsma and Hilde Heijink",
year = "2019",
doi = "10.1007/978-3-319-98143-7_9",
language = "English",
series = "Molecular and Translational Medicine",
publisher = "Humana Press",
pages = "239--270",
editor = "Monte Willis and Yates, {Cecelia C. } and Schisler, {Jonathan C. }",
booktitle = "Fibrosis in Disease",
edition = "1",

}

RIS

TY - CHAP

T1 - Dynamic Reciprocity

T2 - The Role of the Extracellular Matrix Microenvironment in Amplifying and Sustaining Pathological Lung Fibrosis

AU - Burgess, Janette

AU - Muizer, Kirsten

AU - Brandsma, C.

AU - Heijink, Hilde

PY - 2019

Y1 - 2019

N2 - When taken together fibrotic lung diseases are the leading cause of mortality worldwide, but our understanding of the underlying mechanisms driving these processes is limited. The lung consists of defined parts including the airways and parenchyma. The principal building blocks of these parts are the extracellular matrix (ECM). The ECM supports cells structurally while also acting as a bioactive environment directing cellular responses during pathological events in the lung. Airway and parenchymal tissue ECM alterations characterize the changes identified in many fibrotic lung diseases, including in asthma, chronic obstructive pulmonary disease (COPD), and idiopathic pulmonary fibrosis (IPF). Characterization of the profiles of changes and investigation into how these ECM changes contribute to the disease process has been the recent focus within the field. Studies suggest that the changes in the composition, organization, and stiffness of the ECM environment in the lung may drive functional responses of cells and thereby contribute to the pathological outcome. This chapter aims to summarize the state of the art regarding the dynamic interchange of the ECM in pulmonary fibrotic diseases and the approaches for modulating these aberrations in the future. The overarching goal is to expand knowledge of the contributions of the ECM to enable a better understanding of fibrotic lung diseases and to identify novel approaches for therapeutic targeting in this area.

AB - When taken together fibrotic lung diseases are the leading cause of mortality worldwide, but our understanding of the underlying mechanisms driving these processes is limited. The lung consists of defined parts including the airways and parenchyma. The principal building blocks of these parts are the extracellular matrix (ECM). The ECM supports cells structurally while also acting as a bioactive environment directing cellular responses during pathological events in the lung. Airway and parenchymal tissue ECM alterations characterize the changes identified in many fibrotic lung diseases, including in asthma, chronic obstructive pulmonary disease (COPD), and idiopathic pulmonary fibrosis (IPF). Characterization of the profiles of changes and investigation into how these ECM changes contribute to the disease process has been the recent focus within the field. Studies suggest that the changes in the composition, organization, and stiffness of the ECM environment in the lung may drive functional responses of cells and thereby contribute to the pathological outcome. This chapter aims to summarize the state of the art regarding the dynamic interchange of the ECM in pulmonary fibrotic diseases and the approaches for modulating these aberrations in the future. The overarching goal is to expand knowledge of the contributions of the ECM to enable a better understanding of fibrotic lung diseases and to identify novel approaches for therapeutic targeting in this area.

U2 - 10.1007/978-3-319-98143-7_9

DO - 10.1007/978-3-319-98143-7_9

M3 - Chapter

T3 - Molecular and Translational Medicine

SP - 239

EP - 270

BT - Fibrosis in Disease

A2 - Willis, Monte

A2 - Yates, Cecelia C.

A2 - Schisler, Jonathan C.

PB - Humana Press

ER -

ID: 77507914