Cell phenotype as a target of drug therapy in chronic inflammatory diseases

Abstract 

Many diseases share common pathological changes which could in principle be targets for new drugs. Vascular leakage of plasma and migration of cells into perivascular tissues are common to chronic inflammatory diseases such as asthma, atherosclerosis, arthritis, and proliferative nephropathy as well as some non-inflammatory proliferative disorders such as diabetes mellitis. Individual components of plasma have been shown to stimulate cellular proliferation, matrix deposition and phenotypic change, leading to tissue-damaging structural changes. Whereas most anti-inflammatory drugs either downregulate expression of inflammatory mediators or inhibit their actions on cells, there are alternate potential therapeutic strategies described here based on moderating vascular leakage or its consequences in chronic diseases. The hypothesis is that drugs that can modify a cell’s phenotype could be used to limit structural changes which accompany inflammation and thus reduce permanent debility resulting from these diseases. Such drugs include the differentiating agents being developed for cancer therapy.

No full text is available. To read the body of this article, please view the PDF online.