Literature DB >> 25372762

Podocytes: recent biomolecular developments.

Silvia Armelloni, Alessandro Corbelli, Laura Giardino, Min Li, Masami Ikehata, Deborah Mattinzoli, Piergiorgio Messa, Chiara Pignatari, Shojiro Watanabe, Maria Pia Rastaldi.   

Abstract

Podocytes are postmitotic renal glomerular cells with multiple ramifications that extend from the cell body. Processes departing from a podocyte interdigitate with corresponding projections from neighboring cells and form an intricate web that enwraps the glomerular capillary completely. Podocyte processes are interconnected by the slit diaphragm, an adhesion junction mostly formed by Ig-like molecules, cadherins/protocadherins, ephrin/eph, and neurexin molecules organized in an assembly that resembles synaptic junctions. Podocyte failure is primarily or secondarily implicated in all forms of proteinuric glomerular diseases, as confirmed by the morphological changes of their elaborate cell architecture detectable by electron microscopy. Importantly, mutations of podocyte proteins are responsible for the most severe forms of congenital nephrotic syndrome. In the last 15 years, progressive technological advances have aided the study of podocyte biology and pathology, confirming the relevance of podocyte molecules and signaling pathways for the function of the glomerular filter. This review will examine the most important and newest discoveries in the field, which is rapidly evolving, hopefully leading to a detailed knowledge of this fascinating cell and to the development of specific therapeutic options for proteinuric diseases.

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Year:  2014        PMID: 25372762     DOI: 10.1515/bmc-2014-0020

Source DB:  PubMed          Journal:  Biomol Concepts        ISSN: 1868-5021


  7 in total

1.  Disease-causing mutations of RhoGDIα induce Rac1 hyperactivation in podocytes.

Authors:  David Auguste; Mirela Maier; Cindy Baldwin; Lamine Aoudjit; Richard Robins; Indra R Gupta; Tomoko Takano
Journal:  Small GTPases       Date:  2016-01-04

2.  MicroRNA-145-5p attenuates high glucose-induced apoptosis by targeting the Notch signaling pathway in podocytes.

Authors:  Bing Wei; Yi-Song Liu; Hai-Xia Guan
Journal:  Exp Ther Med       Date:  2020-01-07       Impact factor: 2.447

Review 3.  Nanomedicines for renal disease: current status and future applications.

Authors:  Nazila Kamaly; John C He; Dennis A Ausiello; Omid C Farokhzad
Journal:  Nat Rev Nephrol       Date:  2016-10-31       Impact factor: 28.314

4.  TRIM32 Inhibition Attenuates Apoptosis, Oxidative Stress, and Inflammatory Injury in Podocytes Induced by High Glucose by Modulating the Akt/GSK-3β/Nrf2 Pathway.

Authors:  Zhao Chen; Lifang Tian; Li Wang; Xiaotao Ma; Fuqian Lei; Xianghui Chen; Rongguo Fu
Journal:  Inflammation       Date:  2021-11-16       Impact factor: 4.092

5.  NUP160 knockdown inhibits the progression of diabetic nephropathy in vitro and in vivo.

Authors:  Jiayong Xie; Zhi Chen; Gang Yao; Ying Yuan; Wenjuan Yu; Qiang Zhu
Journal:  Regen Ther       Date:  2022-06-17       Impact factor: 3.651

6.  FAM40A alters the cytoskeleton of podocytes in familial focal and segmental glomerulosclerosis by regulating F-actin and nephrin.

Authors:  Zhou Chen; Yinghui Zhang; Xuezhi Zhao
Journal:  Arch Med Sci       Date:  2018-02-02       Impact factor: 3.318

7.  Ginsenoside Rg1 Alleviates Podocyte EMT Passage by Regulating AKT/GSK3 β/β-Catenin Pathway by Restoring Autophagic Activity.

Authors:  Yimin Shi; Yanbin Gao; Tao Wang; Xiaolei Wang; Jiaxin He; Jiayi Xu; Bingjie Wu; Yimeng Li
Journal:  Evid Based Complement Alternat Med       Date:  2020-01-30       Impact factor: 2.629

  7 in total

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