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Letter

Response to 'Ramipril attenuates lipid peroxidation and cardiac fibrosis in an experimental model of rheumatoid arthritis'

Di Wang, Shanshan Hu and Wei Wei*

Author affiliations

Institute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-inflammatory and Immunopharmacology of China Education Ministry, Hefei 230032, Anhui Province, PR China

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Citation and License

Arthritis Research & Therapy 2013, 15:405  doi:10.1186/ar4195


See related research by Shi et al., http://arthritis-research.com/content/14/5/R223, and related letter by Shi et al., http://arthritis-research.com/content/15/2/406

Published: 3 April 2013

First paragraph (this article has no abstract)

We read with great interest the recent issue of Arthritis Research & Therapy in which Shi and colleagues [1] investigated the effects of ramipril on oxidative stress and fibrosis in the heart of rats with adjuvant arthritis. The authors concluded that ramipril reversed arthritis scoring and decreased markers of oxidative stress, inflammation, and tissue fibrosis. Undoubtedly, their findings will promote the attempt to diminish the cardiovascular risk of patients with rheumatoid arthritis (RA) by using angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) or both.