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Published ahead of print on May 21, 2009
J Am Soc Nephrol 20: 1179-1187, 2009
© 2009 American Society of Nephrology
doi: 10.1681/ASN.2008050549
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Brief Review

The Mesangial Cell Revisited: No Cell Is an Island

Detlef Schlöndorff* and Bernhard Banas{dagger}

* Mount Sinai School of Medicine, Division of Nephrology, New York, New York; and {dagger} Department of Internal Medicine II, Nephrology, University of Regensburg, Regensburg, Germany

Correspondence: Dr. Detlef Schlöndorff, Mount Sinai School of Medicine, Samuel Bronfman Department of Medicine, Division of Nephrology, One Gustave L. Levy Place, Box 1243, New York, NY 10029-6574. Phone: 212-241-2977; Fax: 212-849-2643; E-mail: detlef.schlondorff{at}mssm.edu

Mesangial cells and their matrix form the central stalk of the glomerulus and are part of a functional unit interacting closely with endothelial cells and podocytes. Alterations in one cell type can produce changes in the others. The cytokines generated by mesangial cells, endothelial cells, and podocytes that tridirectionally and interactively influence cognate receptors on receiver cells are not fully defined. The existence of cytokine cross-talk seems very likely, given the observations that podocyte injury frequently results in mesangial cell proliferation, whereas mesangial cell injury leads to foot process fusion and proteinuria. Another potentially fruitful area of future research is the role of mesangial cells as local modulators of innate and adaptive immune responses. Thus, mesangial cell research still holds much promise.






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Copyright © 2009 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673