Renal tubular epithelial cells: the neglected mediator of tubulointerstitial fibrosis after injury

Renal fibrosis, especially tubulointerstitial fibrosis, is the inevitable outcome of all progressive chronic kidney diseases (CKDs) and exerts a great health burden worldwide. For a long time, interests in renal fibrosis have been concentrated on fibroblasts and myofibroblasts. However, in recent ye...

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Published inCell death & disease Vol. 9; no. 11; pp. 1126 - 11
Main Authors Qi, Ruochen, Yang, Cheng
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 13.11.2018
Springer Nature B.V
Subjects
631/250/256
692/699/1585/104/1586
96/21
Animals
Antibodies
Biochemistry
Biomedical and Life Sciences
Cell Biology
Cell Communication - immunology
Cell Culture
Cytokines - genetics
Cytokines - immunology
Epithelial cells
Epithelial Cells - immunology
Epithelial Cells - pathology
Fibroblasts
Fibrosis
Gene Expression Regulation
Humans
Immunology
Inflammasomes - genetics
Inflammasomes - immunology
Kidney Tubules - immunology
Kidney Tubules - pathology
Life Sciences
Mitochondria - immunology
Mitochondria - pathology
Monocytes - immunology
Monocytes - pathology
Myofibroblasts - immunology
Myofibroblasts - pathology
Nephritis, Interstitial - genetics
Nephritis, Interstitial - immunology
Nephritis, Interstitial - pathology
NLR Family, Pyrin Domain-Containing 3 Protein - genetics
NLR Family, Pyrin Domain-Containing 3 Protein - immunology
Review
Review Article
Signal Transduction
Online AccessGet full text

Cover

Abstract Renal fibrosis, especially tubulointerstitial fibrosis, is the inevitable outcome of all progressive chronic kidney diseases (CKDs) and exerts a great health burden worldwide. For a long time, interests in renal fibrosis have been concentrated on fibroblasts and myofibroblasts. However, in recent years, growing numbers of studies have focused on the role of tubular epithelial cells (TECs). TECs, rather than a victim or bystander, are probably a neglected mediator in renal fibrosis, responding to a variety of injuries. The maladaptive repair mechanisms of TECs may be the key point in this process. In this review, we will focus on the role of TECs in tubulointerstitial fibrosis. We will follow the fate of a tubular cell and depict the intracellular changes after injury. We will then discuss how the repair mechanism of tubular cells becomes maladaptive, and we will finally discuss the intercellular crosstalk in the interstitium that ultimately proceeds tubulointerstitial fibrosis.
AbstractList Renal fibrosis, especially tubulointerstitial fibrosis, is the inevitable outcome of all progressive chronic kidney diseases (CKDs) and exerts a great health burden worldwide. For a long time, interests in renal fibrosis have been concentrated on fibroblasts and myofibroblasts. However, in recent years, growing numbers of studies have focused on the role of tubular epithelial cells (TECs). TECs, rather than a victim or bystander, are probably a neglected mediator in renal fibrosis, responding to a variety of injuries. The maladaptive repair mechanisms of TECs may be the key point in this process. In this review, we will focus on the role of TECs in tubulointerstitial fibrosis. We will follow the fate of a tubular cell and depict the intracellular changes after injury. We will then discuss how the repair mechanism of tubular cells becomes maladaptive, and we will finally discuss the intercellular crosstalk in the interstitium that ultimately proceeds tubulointerstitial fibrosis.
Renal fibrosis, especially tubulointerstitial fibrosis, is the inevitable outcome of all progressive chronic kidney diseases (CKDs) and exerts a great health burden worldwide. For a long time, interests in renal fibrosis have been concentrated on fibroblasts and myofibroblasts. However, in recent years, growing numbers of studies have focused on the role of tubular epithelial cells (TECs). TECs, rather than a victim or bystander, are probably a neglected mediator in renal fibrosis, responding to a variety of injuries. The maladaptive repair mechanisms of TECs may be the key point in this process. In this review, we will focus on the role of TECs in tubulointerstitial fibrosis. We will follow the fate of a tubular cell and depict the intracellular changes after injury. We will then discuss how the repair mechanism of tubular cells becomes maladaptive, and we will finally discuss the intercellular crosstalk in the interstitium that ultimately proceeds tubulointerstitial fibrosis.Renal fibrosis, especially tubulointerstitial fibrosis, is the inevitable outcome of all progressive chronic kidney diseases (CKDs) and exerts a great health burden worldwide. For a long time, interests in renal fibrosis have been concentrated on fibroblasts and myofibroblasts. However, in recent years, growing numbers of studies have focused on the role of tubular epithelial cells (TECs). TECs, rather than a victim or bystander, are probably a neglected mediator in renal fibrosis, responding to a variety of injuries. The maladaptive repair mechanisms of TECs may be the key point in this process. In this review, we will focus on the role of TECs in tubulointerstitial fibrosis. We will follow the fate of a tubular cell and depict the intracellular changes after injury. We will then discuss how the repair mechanism of tubular cells becomes maladaptive, and we will finally discuss the intercellular crosstalk in the interstitium that ultimately proceeds tubulointerstitial fibrosis.
ArticleNumber 1126
Author Yang, Cheng
Qi, Ruochen
Author_xml – sequence: 1
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  surname: Qi
  fullname: Qi, Ruochen
  organization: Department of Urology, Zhongshan Hospital, Fudan University, Shanghai Medical College, Fudan University
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  givenname: Cheng
  surname: Yang
  fullname: Yang, Cheng
  email: esuperyc@163.com, yang.cheng1@zs-hospital.sh.cn
  organization: Department of Urology, Zhongshan Hospital, Fudan University, Shanghai Key Laboratory of Organ Transplantation
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Issue 11
Language English
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  doi: 10.1371/journal.pone.0070464
– volume: 42
  start-page: 453
  year: 2018
  ident: 1157_CR55
  publication-title: Int. J. Mol. Med.
– volume: 50
  start-page: 1
  year: 2017
  ident: 1157_CR3
  publication-title: Med. Mol. Morphol.
  doi: 10.1007/s00795-016-0146-3
– volume: 7
  start-page: 25604
  year: 2016
  ident: 1157_CR78
  publication-title: Oncotarget
  doi: 10.18632/oncotarget.8238
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Snippet Renal fibrosis, especially tubulointerstitial fibrosis, is the inevitable outcome of all progressive chronic kidney diseases (CKDs) and exerts a great health...
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SubjectTerms 631/250/256
692/699/1585/104/1586
96/21
Animals
Antibodies
Biochemistry
Biomedical and Life Sciences
Cell Biology
Cell Communication - immunology
Cell Culture
Cytokines - genetics
Cytokines - immunology
Epithelial cells
Epithelial Cells - immunology
Epithelial Cells - pathology
Fibroblasts
Fibrosis
Gene Expression Regulation
Humans
Immunology
Inflammasomes - genetics
Inflammasomes - immunology
Kidney Tubules - immunology
Kidney Tubules - pathology
Life Sciences
Mitochondria - immunology
Mitochondria - pathology
Monocytes - immunology
Monocytes - pathology
Myofibroblasts - immunology
Myofibroblasts - pathology
Nephritis, Interstitial - genetics
Nephritis, Interstitial - immunology
Nephritis, Interstitial - pathology
NLR Family, Pyrin Domain-Containing 3 Protein - genetics
NLR Family, Pyrin Domain-Containing 3 Protein - immunology
Review
Review Article
Signal Transduction
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Title Renal tubular epithelial cells: the neglected mediator of tubulointerstitial fibrosis after injury
URI https://link.springer.com/article/10.1038/s41419-018-1157-x
https://www.ncbi.nlm.nih.gov/pubmed/30425237
https://www.proquest.com/docview/2132701969
https://www.proquest.com/docview/2133429100
https://pubmed.ncbi.nlm.nih.gov/PMC6233178
Volume 9
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