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足细胞 TRPC 通道的调节——探寻肾小球疾病治疗的新靶点。

TRPC channel modulation in podocytes-inching toward novel treatments for glomerular disease.

机构信息

Department of Medicine, Division of Nephrology and Hypertension, Leonard Miller School of Medicine, University of Miami, Miami, FL, USA.

出版信息

Pediatr Nephrol. 2011 Jul;26(7):1057-64. doi: 10.1007/s00467-010-1718-4. Epub 2010 Dec 16.

DOI:10.1007/s00467-010-1718-4
PMID:21161284
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3098353/
Abstract

Glomerular kidney disease is a major healthcare burden and considered to represent a sum of disorders that evade a refined and effective treatment. Excellent biological and genetic studies have defined pathways that go awry in podocytes, which are the regulatory cells of the glomerular filter. The question now is how to define targets for novel improved therapies. In this review, we summarize critical points around targeting the TRPC6 channel in podocytes.

摘要

肾小球肾病是一个主要的医疗保健负担，被认为是一系列逃避精细和有效治疗的疾病的总和。优秀的生物学和遗传学研究已经确定了足细胞中出错的途径，足细胞是肾小球滤过器的调节细胞。现在的问题是如何确定新型改良疗法的靶点。在这篇综述中，我们总结了针对足细胞中的 TRPC6 通道的靶向治疗的关键点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95db/3098353/43785d0252b2/467_2010_1718_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95db/3098353/bb4bd781ee47/467_2010_1718_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95db/3098353/85e790c7fca9/467_2010_1718_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95db/3098353/43785d0252b2/467_2010_1718_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95db/3098353/bb4bd781ee47/467_2010_1718_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95db/3098353/85e790c7fca9/467_2010_1718_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95db/3098353/43785d0252b2/467_2010_1718_Fig3_HTML.jpg

相似文献

[1]
TRPC channel modulation in podocytes-inching toward novel treatments for glomerular disease.

Pediatr Nephrol. 2010-12-16

[2]
Angiotensin II has acute effects on TRPC6 channels in podocytes of freshly isolated glomeruli.

Kidney Int. 2014-9

[3]
Transient receptor potential channel 6 (TRPC6) protects podocytes during complement-mediated glomerular disease.

J Biol Chem. 2013-11-5

[4]
Regulation of TRPC6 ion channels in podocytes - Implications for focal segmental glomerulosclerosis and acquired forms of proteinuric diseases.

Acta Physiol Hung. 2015-9

[5]
TRPC6 channel as an emerging determinant of the podocyte injury susceptibility in kidney diseases.

Am J Physiol Renal Physiol. 2015-9-1

[6]
Podocyte-specific overexpression of wild type or mutant trpc6 in mice is sufficient to cause glomerular disease.

PLoS One. 2010-9-20

[7]
TRPC6 mutations associated with focal segmental glomerulosclerosis cause constitutive activation of NFAT-dependent transcription.

Am J Physiol Cell Physiol. 2009-3

[8]
TRPC6 channels and their binding partners in podocytes: role in glomerular filtration and pathophysiology.

Am J Physiol Renal Physiol. 2010-8-4

[9]
Vitamin D down-regulates TRPC6 expression in podocyte injury and proteinuric glomerular disease.

Am J Pathol. 2013-2-4

[10]
Angiotensin II contributes to podocyte injury by increasing TRPC6 expression via an NFAT-mediated positive feedback signaling pathway.

Am J Pathol. 2011-8-11

引用本文的文献

[1]
TRPC Channels in Proteinuric Kidney Diseases.

Cells. 2019-12-23

[2]
Pharmacological inhibition of focal segmental glomerulosclerosis-related, gain of function mutants of TRPC6 channels by semi-synthetic derivatives of larixol.

Br J Pharmacol. 2017-10-15

[3]
Enhanced expression of transient receptor potential channel 3 in uterine smooth muscle tissues of lipopolysaccharide-induced preterm delivery mice.

Iran J Basic Med Sci. 2016-5

[4]
Podocyte Purinergic P2X4 Channels Are Mechanotransducers That Mediate Cytoskeletal Disorganization.

J Am Soc Nephrol. 2016-3

[5]
Gq signaling causes glomerular injury by activating TRPC6.

J Clin Invest. 2015-5

[6]
A novel TRPC6 mutation in a family with podocytopathy and clinical variability.

BMC Nephrol. 2013-5-10

[7]
Membrane trafficking in podocyte health and disease.

Pediatr Nephrol. 2012-8-30

本文引用的文献

[1]
Establishment of protein delivery systems targeting podocytes.

PLoS One. 2010-7-29

[2]
TRPC6 channels and their binding partners in podocytes: role in glomerular filtration and pathophysiology.

Am J Physiol Renal Physiol. 2010-8-4

[3]
Novel siRNA delivery system to target podocytes in vivo.

PLoS One. 2010-3-1

[4]
Autophagy influences glomerular disease susceptibility and maintains podocyte homeostasis in aging mice.

J Clin Invest. 2010-4

[5]
Toward the development of podocyte-specific drugs.

Kidney Int. 2010-2-3

[6]
A novel TRPC6 mutation that causes childhood FSGS.

PLoS One. 2009-11-10

[7]
Transient receptor potential channels on sensory nerves.

Handb Exp Pharmacol. 2009

[8]
M-type phospholipase A2 receptor as target antigen in idiopathic membranous nephropathy.

N Engl J Med. 2009-7-2

[9]
Signaling in regulation of podocyte phenotypes.

Nephron Physiol. 2009

[10]
TRPC6 mutations associated with focal segmental glomerulosclerosis cause constitutive activation of NFAT-dependent transcription.

Am J Physiol Cell Physiol. 2009-3

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