Models of liver fibrosis: exploring the dynamic nature of inflammation and repair in a solid organ.

By J. Iredale. Journal of Clinical Investigation, 2007

908 citations recorded by the source corpus.

Subfields: Epidemiology, Hepatology, Immunology

View Paper: https://www.semanticscholar.org/paper/81f2477e42002b8dc9c39cfa0f3612a686fb509e

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. Natascha Roehlen
2. E. Crouchet
3. T. Baumert
4. TA Wynn
5. Luke Barron
6. P. Newsome
7. S. Friedman
8. B. Hinz

In Hepatology

1. T. Baumert
2. Natascha Roehlen
3. E. Crouchet
4. TA Wynn
5. Luke Barron
6. S. Friedman
7. B. Hinz
8. Y. Saiman

In Immunology

1. Luke Barron
2. Natascha Roehlen
3. S. Friedman
4. B. Hinz
5. E. Crouchet
6. TA Wynn
7. T. Baumert

Citations in the corpus

• Pathogenesis of non-alcoholic fatty liver disease (2009, background): “The pathogenesis of fibrosis is not within the remit of this review and is well covered elsewhere.(95) There are certain aspects of liver fibrosis and repair which are relatively specific to NASH and are worth considering here.”
• Liver Fibrosis: Mechanistic Concepts and Therapeutic Perspectives (2020, background): “destroys the physiological architecture of the liver [7].”
• Hepatic Stellate Cells and Liver Fibrosis (2013, neutral): “Changes in the composition and stiffness of ECM also impact on stellate cell responses (84, 121, 315) suggesting a feed-forward loop where stellate cell mediated changes in ECM further drive stellate cell activation.”
• Cellular and molecular mechanisms of fibrosis (2008, background): “Thus, ongoing inflammation might be required for the successful resolution of fibrotic disease [166].”
• Remodeling and homeostasis of the extracellular matrix: implications for fibrotic diseases and cancer (2011, neutral): “In such situations, the balance of matrix production and degradation tips in favor of production, which can be facilitated by overexpression of TIMPs or loss of MMP expression, resulting in incomplete matrix remodeling and irreversible fibrosis (Issa et al., 2004).”
• Macrophages: Master Regulators of Inflammation and Fibrosis (2010, background): “However, phagocytosis by macrophages can also aid in the regression or resolution of fibrosis because clearing apoptotic myofibroblasts, hepatocytes, and cellular debris often eliminates the stimuli inducing TGF-b1 and other profibrotic factors.(2,24) The macrophage-dependent proinflammatory respons”
• Evolving challenges in hepatic fibrosis (2010, background): “Fibrosis that develops in weeks in rodents does not completely mimic the slow evolution of fibrosis in humans, particularly with respect to the amount of ECM crosslinking and loss of cellularity that occurs over longer intervals in humans”
• The myofibroblast: paradigm for a mechanically active cell. (2010, background): “Myofibroblast-generated contractures are also fundamental in organ fibrosis, affecting liver (Gressner and Weiskirchen, 2006; Iredale, 2007), heart (Baudino et al., 2006; Brown R.D. et al., 2005), lung (Phan, 2002; Thannickal et al., 2004) and kidney (Liu, 2006) with often lethal consequences.”
• Integrating mechanisms of pulmonary fibrosis (2011, neutral): “JEM Vol. 208, No. 7 1343 Review by facilitating the recruitment of bone marrow–derived collagen–secreting fibrocytes to the lung (Phillips et al., 2004; Moore et al., 2005, 2006).”