Affiliation:
1. Department of Medicine, Department of Anatomy and Cell Biology, and Department of Physiology and Cellular Biophysics, Columbia University, New York, NY 10032, USA.
2. Department of Cellular and Molecular Medicine and Department of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093–0651, USA.
Abstract
A number of widespread and devastating chronic diseases, including atherosclerosis, type 2 diabetes, and Alzheimer’s disease, have a pathophysiologically important inflammatory component. In these diseases, the precise identity of the inflammatory stimulus is often unknown and, if known, is difficult to remove. Thus, there is interest in therapeutically targeting the inflammatory response. Although there has been success with anti-inflammatory therapy in chronic diseases triggered by primary inflammation dysregulation or autoimmunity, there are considerable limitations. In particular, the inflammatory response is critical for survival. As a result, redundancy, compensatory pathways, and necessity narrow the risk:benefit ratio of anti-inflammatory drugs. However, new advances in understanding inflammatory signaling and its links to resolution pathways, together with new drug development, offer promise in this area of translational biomedical research.
Publisher
American Association for the Advancement of Science (AAAS)
Cited by
915 articles.
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