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J Am Soc Nephrol. 2011 Nov;22(11):1969-80. doi: 10.1681/ASN.2011040370. Epub 2011 Oct 6.

Balancing calcium signals through TRPC5 and TRPC6 in podocytes.

Author information

  • 1Division of Nephrology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA. greka.anna@mgh.harvard.edu

Abstract

Calcium (Ca(2+)) ions are important mediators of cellular homeostasis owing to their ability to elicit a dynamic, transient, and tightly regulated range of biochemical responses. More than a decade ago, a nonselective, Ca(2+)-permeable, cationic conductance was identified in podocytes downstream of angiotensin II (Ang II) signaling, but its molecular structure remained elusive. Six years ago, transient receptor potential canonical 6 (TRPC6) mutations were found in families with hereditary FSGS, and TRPC5 and TRPC6 channels are now known as the Ca(2+) influx pathways for this previously described, nonselective, cationic current in podocytes. Ang II activation engages this Ca(2+) influx to modulate the actin cytoskeleton in podocytes. These discoveries dovetail with previously described regulation of actin dynamics by the Ca(2+)-activated phosphatase, calcineurin, and the emergence of Rho GTPases as critical regulators of podocyte function in health and disease. Understanding the interconnected signaling regulated by Ca(2+) currents offers potential new therapeutic targets and highlights the notion that synergistic therapies targeting multiple levels of biochemistry may be useful in treating proteinuric kidney disease.

PMID:
21980113
[PubMed - indexed for MEDLINE]
PMCID:
PMC3231779
Free PMC Article

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