Literature DB >> 33831367

Epithelial proliferation and cell cycle dysregulation in kidney injury and disease.

Kyung Lee1, G Luca Gusella2, John Cijiang He3.   

Abstract

Various cellular insults and injury to renal epithelial cells stimulate repair mechanisms to adapt and restore the organ homeostasis. Renal tubular epithelial cells are endowed with regenerative capacity, which allows for a restoration of nephron function after acute kidney injury. However, recent evidence indicates that the repair is often incomplete, leading to maladaptive responses that promote the progression to chronic kidney disease. The dysregulated cell cycle and proliferation is also a key feature of renal tubular epithelial cells in polycystic kidney disease and HIV-associated nephropathy. Therefore, in this review, we provide an overview of cell cycle regulation and the consequences of dysregulated cell proliferation in acute kidney injury, polycystic kidney disease, and HIV-associated nephropathy. An increased understanding of these processes may help define better targets for kidney repair and combat chronic kidney disease progression.
Copyright © 2021 International Society of Nephrology. All rights reserved.

Entities:  

Keywords:  HIV-associated nephropathy; acute kidney injury; cell cycle; polycystic kidney disease; renal tubular epithelial cells

Mesh:

Year:  2021        PMID: 33831367      PMCID: PMC8855879          DOI: 10.1016/j.kint.2021.03.024

Source DB:  PubMed          Journal:  Kidney Int        ISSN: 0085-2538            Impact factor:   18.998


  173 in total

1.  Nephropathy in human immunodeficiency virus-1 transgenic mice is due to renal transgene expression.

Authors:  L A Bruggeman; S Dikman; C Meng; S E Quaggin; T M Coffman; P E Klotman
Journal:  J Clin Invest       Date:  1997-07-01       Impact factor: 14.808

2.  Intrinsic epithelial cells repair the kidney after injury.

Authors:  Benjamin D Humphreys; M Todd Valerius; Akio Kobayashi; Joshua W Mugford; Savuth Soeung; Jeremy S Duffield; Andrew P McMahon; Joseph V Bonventre
Journal:  Cell Stem Cell       Date:  2008-03-06       Impact factor: 24.633

3.  The dysregulated podocyte phenotype: a novel concept in the pathogenesis of collapsing idiopathic focal segmental glomerulosclerosis and HIV-associated nephropathy.

Authors:  L Barisoni; W Kriz; P Mundel; V D'Agati
Journal:  J Am Soc Nephrol       Date:  1999-01       Impact factor: 10.121

4.  Repair of injured proximal tubule does not involve specialized progenitors.

Authors:  Benjamin D Humphreys; Suzanne Czerniak; Derek P DiRocco; Wirasat Hasnain; Rabia Cheema; Joseph V Bonventre
Journal:  Proc Natl Acad Sci U S A       Date:  2011-05-16       Impact factor: 11.205

5.  Mitigation of acute kidney injury by cell-cycle inhibitors that suppress both CDK4/6 and OCT2 functions.

Authors:  Navjotsingh Pabla; Alice A Gibson; Mike Buege; Su Sien Ong; Lie Li; Shuiying Hu; Guoqing Du; Jason A Sprowl; Aksana Vasilyeva; Laura J Janke; Eberhard Schlatter; Taosheng Chen; Giuliano Ciarimboli; Alex Sparreboom
Journal:  Proc Natl Acad Sci U S A       Date:  2015-04-06       Impact factor: 11.205

6.  Growth Pattern of Kidney Cyst Number and Volume in Autosomal Dominant Polycystic Kidney Disease.

Authors:  Kyongtae T Bae; Wen Zhou; Chengli Shen; Douglas P Landsittel; Zhiyuan Wu; Cheng Tao; Arlene B Chapman; Vicente E Torres; Alan S L Yu; Michal Mrug; William M Bennett; Peter C Harris
Journal:  Clin J Am Soc Nephrol       Date:  2019-05-14       Impact factor: 8.237

7.  Deletion of podocyte STAT3 mitigates the entire spectrum of HIV-1-associated nephropathy.

Authors:  Leyi Gu; Yan Dai; Jin Xu; Sandeep Mallipattu; Lewis Kaufman; Paul E Klotman; John C He; Peter Y Chuang
Journal:  AIDS       Date:  2013-04-24       Impact factor: 4.177

8.  Essential role for a novel population of binucleated mammary epithelial cells in lactation.

Authors:  Anne C Rios; Nai Yang Fu; Paul R Jamieson; Bhupinder Pal; Lachlan Whitehead; Kevin R Nicholas; Geoffrey J Lindeman; Jane E Visvader
Journal:  Nat Commun       Date:  2016-04-22       Impact factor: 14.919

9.  Promiscuous Targeting of Cellular Proteins by Vpr Drives Systems-Level Proteomic Remodeling in HIV-1 Infection.

Authors:  Edward J D Greenwood; James C Williamson; Agata Sienkiewicz; Adi Naamati; Nicholas J Matheson; Paul J Lehner
Journal:  Cell Rep       Date:  2019-04-30       Impact factor: 9.423

Review 10.  Vpr and Its Cellular Interaction Partners: R We There Yet?

Authors:  Helena Fabryova; Klaus Strebel
Journal:  Cells       Date:  2019-10-24       Impact factor: 6.600

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  5 in total

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Authors:  Kan Li; Li Gao; Sen Zhou; Yan-Rong Ma; Xiao Xiao; Qian Jiang; Zhi-Hong Kang; Ming-Long Liu; Tian-Xi Liu
Journal:  Mol Cell Biochem       Date:  2022-08-24       Impact factor: 3.842

2.  Proximal tubule cyclophilin D mediates kidney fibrogenesis in obstructive nephropathy.

Authors:  Hee-Seong Jang; Mi Ra Noh; Ligyeom Ha; Jinu Kim; Babu J Padanilam
Journal:  Am J Physiol Renal Physiol       Date:  2021-08-16

3.  A novel de novo truncating TRIM8 variant associated with childhood-onset focal segmental glomerulosclerosis without epileptic encephalopathy: a case report.

Authors:  Yoko Shirai; Kenichiro Miura; Naoto Kaneko; Kiyonobu Ishizuka; Amane Endo; Taeko Hashimoto; Shoichiro Kanda; Yutaka Harita; Motoshi Hattori
Journal:  BMC Nephrol       Date:  2021-12-20       Impact factor: 2.388

4.  Control of Directed Cell Migration after Tubular Cell Injury by Nucleotide Signaling.

Authors:  Sabrina Gessler; Clara Guthmann; Vera Schuler; Miriam Lilienkamp; Gerd Walz; Toma Antonov Yakulov
Journal:  Int J Mol Sci       Date:  2022-07-17       Impact factor: 6.208

5.  Tubular IKKβ Deletion Alleviates Acute Ischemic Kidney Injury and Facilitates Tissue Regeneration.

Authors:  Eileen Dahlke; Toni Engmann; Yaman Anan; Robert Häsler; Giovanni Solinas; Franziska Theilig
Journal:  Int J Mol Sci       Date:  2022-09-05       Impact factor: 6.208

  5 in total

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