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10.1007/s00467-015-3224-1

http://scihub22266oqcxt.onion/10.1007/s00467-015-3224-1
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suck abstract from ncbi


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pmid26490951      Pediatr+Nephrol 2016 ; 31 (ä): 1047-54
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  • Calcium, TRPC channels, and regulation of the actin cytoskeleton in podocytes: towards a future of targeted therapies #MMPMID26490951
  • Wieder N; Greka A
  • Pediatr Nephrol 2016[]; 31 (ä): 1047-54 PMID26490951show ga
  • With more than 6,000 new pediatric patients with treatment-resistant nephrotic syndrome in the US each year alone, the unmet need for novel, podocyte-specific therapies is substantial. Recently, the established therapeutic benefit of angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARB) was used as a starting point to gain insight into the pathomechanism of primary podocytopathies. A calcium (Ca2+)-mediated pathway has been identified that connects the angiotensin type 1 receptor (AT1R) to podocyte cytoskeletal dynamics, essential for a functioning glomerular filtration barrier. This discovery provided an important missing piece in our understanding of the pathomechanism of filter barrier damage, revealing Ca2+ signaling as critical for podocyte health and disease. The identification of the two Ca2+ permeant channels TRPC5 and TRPC6 as mediators of this pathway not only bolstered the importance of podocyte cytoskeleton dynamics but also revealed promising drug targets for treatment-resistant nephrotic syndrome. This review will focus on this novel signaling pathway in primary podocytopathies and its implications for next-generation therapies for glomerular disease.
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