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Vol. 304, Issue 3, 905-912, March 2003
Laboratory of Molecular Carcinogenesis, National Institute of
Environmental Health Sciences, Research Triangle Park, North Carolina
(P.A.N.); and Department of Pharmaceutical Sciences, Medical University
of South Carolina, Charleston, South Carolina (R.G.S.)
In many cases, acute renal failure (ARF) is the result of proximal
tubular cell injury and death and can arise in a variety of clinical
situations, especially following renal ischemia and drug or toxicant
exposure. Although much research has focused on the cellular events
leading to ARF, less emphasis has been placed on the mechanisms of
renal cell repair and regeneration, although ARF is reversed in over
half of those who acquire it. Studies using in vivo and in vitro models
have demonstrated the importance of proliferation, migration, and
repair of physiological functions of injured renal proximal tubular
cells (RPTC) in the reversal of ARF. Growth factors have been shown to
produce migration and proliferation of injured RPTC, although the
specific mechanisms through which growth factors promote renal
regeneration in vivo are unclear. Recently, interactions between
integrins and extracellular matrix proteins such as collagen IV were
shown to promote the repair of physiological functions in injured RPTC.
Specifically, collagen IV synthesis and deposition following cellular
injury restored integrin polarity and promoted repair of mitochondrial function and active Na+ transport. Furthermore, exogenous
collagen IV, but not collagen I, fibronectin, or laminin, promoted the
repair of physiological functions without stimulating proliferation.
These findings suggest the importance of establishing and/or
maintaining collagen IV-integrin interactions in the stimulation of
repair of physiological functions following sublethal cellular injury.
Furthermore, the pathway that stimulates repair is distinct from that
of proliferation and migration and may be a viable target for
pharmacological intervention.
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