Targeting myosin 1c inhibits murine hepatic fibrogenesis

Author:

Arif Ehtesham12ORCID,Wang Cindy2,Swiderska-Syn Marzena K.3,Solanki Ashish K.1,Rahman Bushra1,Manka Paul P.24,Coombes Jason D.56,Canbay Ali4,Papa Salvatore7,Nihalani Deepak18,Aspichueta Patricia9,Lipschutz Joshua H.110,Syn Wing-Kin2911

Affiliation:

1. Department of Medicine, Nephrology Division, Medical University of South Carolina, Charleston, South Carolina

2. Division of Gastroenterology and Hepatology, Medical University of South Carolina, Charleston, South Carolina

3. Department of Pediatrics, Darby Children’s Research Institute, Hollings Cancer Center, Medical University of South Carolina, Charleston, South Carolina

4. Department of Medicine, University Hospital Knappschaftskrankenhaus, Ruhr-University Bochum, Bochum, Germany

5. Institute of Hepatology, Foundation for Liver Research, London, United Kingdom

6. School of Immunology and Microbial Sciences, Faculty of Life Sciences and Medicine, King's College London, London, United Kingdom

7. Leeds Institute of Medical Research at St. James’s, Faculty of Medicine and Health, University of Leeds, Leeds, United Kingdom

8. Division of Kidney, Urologic and Hematologic Diseases, National Institutes of Health, Bethesda, Maryland

9. Department of Physiology, Faculty of Medicine and Nursing, University of the Basque Country, Universidad del País Vasco/Euskal Herriko Unibertsitatea (UPV/EHU), Leioa, Spain

10. Section of Nephrology, Ralph H Johnson Veterans Affairs Medical Center, Charleston, South Carolina

11. Section of Gastroenterology, Ralph H Johnson Veterans Affairs Medical Center, Charleston, South Carolina

Abstract

The incidences of liver fibrosis are growing at a rapid pace and have become one of the leading causes of end-stage liver disease. Although TGF-β1 is known to play a prominent role in transforming cells to produce excessive extracellular matrix that lead to hepatic fibrosis, the therapies targeting TGF-β1 have achieved very limited clinical impact. This study highlights motor protein myosin-1c-mediated mechanisms that serve as novel regulators of TGF-β1 signaling and fibrosis

Funder

HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases

U.S. Department of Veterans Affairs

Publisher

American Physiological Society

Subject

Physiology (medical),Gastroenterology,Hepatology,Physiology

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