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Physiology and Pathophysiology of Heme: Implications for Kidney Disease

Michal J. Tracz^*, Jawed Alam and Karl A. Nath^*

^* Division of Nephrology and Hypertension, Mayo Clinic College of Medicine, Rochester, Minnesota; and Department of Molecular Genetics, Alton Ochsner Medical Center, New Orleans, Louisiana

Address correspondence to: Dr. Karl A. Nath, Mayo Clinic, 200 First Street, SW, Guggenheim 542, Rochester, MN 55905. Phone: 507-284-1646; Fax: 507-284-3757; nath.karl{at}mayo.edu

An iron-containing, tetrapyrrole ring, heme is an essential prosthetic group in an array of proteins that comprehensively affect cellular function and metabolism; yet "free" heme in sufficient amounts can be damaging to the kidney and other organs because of its bioreactivity and pro-oxidant effects. This review discusses the cellular metabolism of heme in health and disease and covers such areas as the synthesis of heme and its utilization in heme proteins; mechanisms underlying the toxicity of heme; and the extent to which pathophysiologic processes, such as renal incorporation of heme proteins or destabilization of intracellular heme proteins, increase intracellular levels of heme and provoke renal injury. The main catabolic process that degrades heme, the heme oxygenase (HO) system, is reviewed, and evidence for the protective effects of HO-1 against acute and chronic heme/heme protein–induced renal injury is summarized. Finally, current views regarding the molecular basis for heme-induced upregulation of HO-1 are discussed.

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Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673