Molecular and Cellular Mechanisms of Treating Fibrosis

Dear Colleagues,

Fibrosis, defined as excessive extracellular matrix (ECM) deposition through persisting myofibroblast activation, is a common and resistant pathologic process, contributing widely to morbidity through organ involvement and increased mortality through the eventual failure of organ systems. Often linked to tissue damage and inflammation at onset, fibrosis currently evades most attempts at therapy, since the established fibrotic lesions have undergone epigenetic and other established secondary changes such as greatly enhanced mechanical stiffness and mechano-sensing. Interstitial lung disease (ILD), cardiac failure, chronic kidney disease, and skin and organ fibrosis in systemic sclerosis are each considered paradigm conditions of complex and resistant fibrosis. Current approaches involve the empirical use of anti-inflammatory or immunosuppressive therapies given during any inflammatory phase, or more specific approaches such as the use of nintedanib which targets receptors for growth factors and angiogenic cytokines, or perfenidone which may inhibit ECM assembly outside of the cell. Improved outcomes can be achieved through the improved early detection of fibrotic changes by the latest imaging and biomarker approaches, or through enhanced understanding of the cellular and molecular mechanisms driving complex fibrosis. Future therapies likely involve targeting key cellular players such as M2-like macrophages, myofibroblasts themselves, or adaptive immune cells, or modification of the ECM itself such as preventing its secretion-stable assembly of fibrillar collagen matrix. Taken together, the clinical problem of fibrosis presents an intriguing conundrum which is likely solvable through modern research approaches and the delivery of targeted therapy.

Dr. Richard Stratton
Guest Editor

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• fibrosis
• systemic sclerosis
• targeted therapy
• extracellular matrix
• collagen
• organ fibrosis
• interstitial lung disease