Calpain 9 as a therapeutic target in TGFβ-induced mesenchymal transition and fibrosis

Author:

Kim David H.12ORCID,Beckett James D.1ORCID,Nagpal Varun1,Seman-Senderos Manuel A.12ORCID,Gould Russell A.13,Creamer Tyler J.4ORCID,MacFarlane Elena Gallo14ORCID,Chen Yichun1ORCID,Bedja Djahida5,Butcher Jonathan T.3ORCID,Mitzner Wayne6ORCID,Rouf Rosanne5ORCID,Hata Shoji7ORCID,Warren Daniel S.4,Dietz Harry C.18ORCID

Affiliation:

1. McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

2. Cellular and Molecular Medicine Program, School of Medicine, Baltimore, MD 21205, USA.

3. Meinig School of Biomedical Engineering, Cornell University, Ithaca, NY 14853, USA.

4. Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

5. Department of Cardiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

6. Department of Environmental Health Sciences, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD 21205, USA.

7. Department of Advanced Science for Biomolecules, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan.

8. Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA.

Abstract

Inhibition of calpain 9, a key mediator of myofibroblast differentiation and tissue fibrosis, protects against fibrosis in preclinical models.

Funder

National Institutes of Health

Howard Hughes Medical Institute

Scleroderma Research Foundation

Charles T. Bauer Foundation

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine

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