Oxides and apoptosis in inflammatory myopathies

✍ Scribed by Martin Stangel; Eilhard Mix; Uwe K. Zettl; Ralf Gold

• Publisher: John Wiley and Sons
• Year: 2001
• Tongue: English
• Weight: 567 KB
• Volume: 55
• Category: Article
• ISSN: 1059-910X
• DOI: 10.1002/jemt.1174

✦ Synopsis

Abstract

Reactive oxygen intermediates (ROI) and nitric oxide (NO^·^) are produced in abundance in the inflammatory muscle diseases of autoimmune origin polymyositis (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 phagocytes in inflammatory myopathies. On the contrary, NO^·^ released at low concentrations at target sites may even have cell‐protective effects. A major mechanism of protection from apoptosis in both myocytes and inflammatory cells seems to be the upregulation of anti‐apoptotic proteins like Bcl‐2. Caution is warranted to apply antioxidative and anti‐apoptotic agents to patients with inflammatory myopathies as long as the pathogenic role of oxides and apoptosis in the individual case is not resolved. Microsc. Res. Tech. 55:249–258, 2001. © 2001 Wiley‐Liss, Inc.