Oxides and apoptosis in inflammatory myopathies

Reactive oxygen intermediates (ROI) and nitric oxide (NO*) are produced in abundance in the inflammatory muscle diseases of autoimmune origin polymyos itis (PM), dermatomyositis (DM), and inclusion body myositis (IBM). However , their role in the pathogenesis of these diseases is so far not clear. In contrast to demyelinating neuropathies, there is no convincing evidence for oxide-induced apoptosis either in myocytes or in lymphocytes and phagocyte s in inflammatory myopathies. On the contrary, NO* released at low concentr ations at target sites may even have cell-protective effects. A major mecha nism of protection from apoptosis in both myocytes and inflammatory cells s eems to be the upregulation of anti-apoptotic proteins like Bcl-2. Caution is warranted to apply antioxidative and anti-apoptotic agents to patients w ith inflammatory myopathies as long as the pathogenic role of oxides and ap optosis in the individual case is not resolved. (C) 2001 Wiley-Liss, Inc.