[Frontiers in Bioscience 13, 4021-4028, May 1, 2008]

Roles of chemokines in renal ischemia/reperfusion injury

Kengo Furuichi1,2, Takashi Wada1, Shuichi Kaneko2, Philip M. Murphy3

1Department of Gastroenterology and Nephrology and 2Division of Blood Purification, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan, 3Molecular Signaling Section, Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA

TABLE OF CONTENTS

1. Abstract
2. Introduction
3. Induction of chemokines after renal ischemia-reperfusion injury
4. Pro-inflammatory cytokines augment inflammation after renal ischemia-reperfusion injury
5. Intracellular signaling pathways linking ischemic injury to chemokine production.
6. Chemokine expression in the injured kidney
7. Temporal and spatial aspects of leukocyte infiltration in renal IR injury
8. Cytokines and chemokines in renal transplantation
9. Anti-inflammatory treatment approaches in renal IR injury
10. Conclusion
11. References
1. ABSTRACT

Ischemia-reperfusion injury (IR) is a common and an important clinical cause of renal disease, such as renal transplantation, renal artery stenosis and following shock from any cause. Inflammatory reaction after IR is regulated by various kinds of mediators. Chemokines are major mediators of the inflammation, and regulate pro-inflammatory cytokine and adhesion molecule expression, and leukocyte infiltration and activation. Chemokines are the key players of inflammation, angiogenesis and fibrosis. These inflammatory processes mediated by chemokines were observed in not only experimental animal models, but also in human renal diseases with ischemic injury. A number of challenges of chemokine targeted therapy is trying to prevent the ischemic injury, and will give some beneficial effect on the injury.