Endogenous Inhibitors of Kidney Inflammation

Abstract

Although inflammation is the physiological response to pathogen invasion and tissue damage, it can also be responsible for significant tissue damage.  Therefore, the inflammatory response must be carefully regulated to prevent critical inflammatory damage to vital organs.  Typically, local endogenous regulatory mechanisms adjust the magnitude of the response such that the injurious condition is resolved and homeostasis is mantained.  Humoral mechanisms that restrain or inhibit inflammation include glucocorticoid hormones, anti-inflammatory cytokines such as IL-10 and transforming growth factor-beta, and soluble cytokine receptors; other mediators facilitate tissue healing, like lipoxins and resolvins.  There is growing evidence that inflammation plays a critical role in the development and progression of heart disease, cancer, stroke, diabetes, kidney diseases, sepsis, and several fibroproliferative disorders.  Consequently, understanding the mechanisms that regulate inflammation may offer therapeutic targets for inhibiting the progression of several diseases.  In this article, we review the significance of several novel endogenous anti-inflammatory mediators in the protection from kidney injury and the potential of these regulatory molecules as therapeutic targets for treatment of kidney inflammatory diseases.

key words: Inflammation, fibrosis, adenosine, inflammatory reflex, Slit.