Myofibroblasts revert to an inactive phenotype during regression of liver fibrosis

By T. Kisseleva, M. Cong, Y. Paik, D. Scholten, Chunyan Jiang, C. Benner, K. Iwaisako, T. Moore-Morris, B. Scott, H. Tsukamoto and 4 more. Proceedings of the National Academy of Sciences of the United States of America, 2012

772 citations recorded by the source corpus.

Subfields: Epidemiology, Hepatology, Immunology

View Paper: https://www.semanticscholar.org/paper/89aba6ddd8f68609fcd900db72fd801f28eee9c1

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. Y. Saiman
2. J. Puche
3. S. Friedman
4. D. Brenner
5. TA Wynn
6. M. Pinzani
7. M. Parola
8. Natascha Roehlen

In Hepatology

1. TA Wynn
2. Y. Saiman
3. J. Puche
4. D. Brenner
5. S. Friedman
6. M. Parola
7. M. Pinzani
8. T. Baumert

In Immunology

1. S. Friedman
2. TA Wynn
3. T. Hunter
4. M. Pinzani
5. D. Brenner
6. D. Sheppard
7. Natascha Roehlen
8. M. Parola

Citations in the corpus

• Cellular and molecular mechanisms in kidney fibrosis. (2014, positive): “Studies of liver disease suggest the equivalent cellular lineage, hepatic stellate cells, can revert to pericytes following resolution of chronic disease in vivo, but are persistently reprogrammed to respond more vigorously to a new injury (69).”
• Vitamin D Receptor-Mediated Stromal Reprogramming Suppresses Pancreatitis and Enhances Pancreatic Cancer Therapy (2014, positive): “Tumor-promoting features are largely restricted to the activated PSC state; the activation process may be reversibleassuggestedby recentwork inhepatic stellatecells (Kisseleva et al., 2012).”
• Hepatic inflammatory responses in liver fibrosis (2023, neutral): “occurs via reversal to a quiescent-like phenotype or complete removal of activated HSCs through apoptosis induction 161,197 .”
• Liver fibrosis: Pathophysiology, pathogenetic targets and clinical issues. (2019, background): “, 2008) or from α-SMA negative precursor cells defined as fibrocytes (Kisseleva et al., 2006).”
• Liver Fibrosis: Mechanistic Concepts and Therapeutic Perspectives (2020, background): “Fibrosis regression is associated with inactivation or apoptosis of HSCs and myofibroblasts [56,232].”
• Liver inflammation and fibrosis. (2017, background): “Hepatic stellate cell differentiation into myofibroblasts is characterized by decreased vitamin A with loss of the adipogenic phenotype (94, 96, 97).”
• Hepatic Stellate Cells and Liver Fibrosis (2013, positive): “now evidence that stellate cells can not only undergo apoptosis, but are also able to either become senescent or revert to a quiescent phenotype (67, 143, 294).”
• Hepatic fibrosis: Concept to treatment. (2015, background): “HSCs, following their activation to myofibroblasts, can revert to an inactivated, albeit not fully quiescent, state [21].”
• Therapy for Fibrotic Diseases: Nearing the Starting Line (2013, background): “Nevertheless, even such “deactivated” cells are primed to more easily reactivate upon recurrent tissue injury (42).”
• Host Responses in Tissue Repair and Fibrosis (2012, background): “However only recently has the fate of HSCs as the major source of myofibroblasts been definitively established (19, 39, 48, 50, 76).”