Role of Transient Receptor Potential Canonical Channel 6 (TRPC6) in Diabetic Kidney Disease by Regulating Podocyte Actin Cytoskeleton Rearrangement

Author:

Wang Qian12ORCID,Tian Xuefei3,Wang Yuyang4,Wang Yan5,Li Jialin12,Zhao Tingting1ORCID,Li Ping1ORCID

Affiliation:

1. Beijing Key Laboratory for Immune-Mediated Inflammatory Diseases, Institute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing 100029, China

2. Beijing University of Chinese Medicine, Beijing 100029, China

3. Section of Nephrology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06510, USA

4. Department of Nephrology, Guang’anmen Hospital of China Academy of Traditional Chinese Medical Sciences, Beijing 100053, China

5. Beijing Key Laboratory of Diabetes Research and Care, Center for Endocrine Metabolism and Immune Diseases, Luhe Hospital, Capital Medical University, Beijing 101149, China

Abstract

Podocyte injury is an important pathogenesis step causing proteinuric kidney diseases such as diabetic kidney disease (DKD). Actin cytoskeleton rearrangement in podocyte induced by multiple pathogenic factors is believed to be the key process resulting in glomerular injury. Many studies have recently shown that transient receptor potential canonical channel 6 (TRPC6) in podocyte plays a critical role in the development and progression of proteinuric kidney disease by regulating its actin cytoskeleton rearrangement. This review is aimed at summarizing the role of TRPC6 on DKD by regulating the podocyte actin cytoskeleton rearrangement, thereby help further broaden our views and understanding on the mechanism of DKD and provide a theoretic basis for exploring new therapeutic targets for DKD patients.

Funder

National Natural Science Foundation of China

Publisher

Hindawi Limited

Subject

Endocrinology,Endocrinology, Diabetes and Metabolism

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