Cited by 130Acute Kidney Injury ResearchCell death mechanisms and regulationRenal Diseases and Glomerulopathies

Pathophysiological role of different tubular epithelial cell death modes in acute kidney injury

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Sancho-Martínez, Sandra M., López-Novoa, José M., López-Hernández, Francisco J.·2015·Clinical Kidney Journal

Abstract

The histological substrate of many forms of intrinsic acute kidney injury (AKI) has been classically attributed to tubular necrosis. However, more recent studies indicate that necrosis is not the main form of cell death in AKI and that other forms such as apoptosis, regulated necrosis (i.e. necroptosis and parthanatos), autophagic cell death and mitotic catastrophe, also participate in AKI and that their contribution depends on the cause and stage of AKI. Herein, we briefly summarize the main characteristics of the major types of cell death and we also critically review the existing evidence on the occurrence of different types of cell death reported in the most common experimental models of AKI and human specimens. We also discuss the pathophysiological mechanisms linking tubule epithelial cell death with reduced glomerular filtration, azotaemia and hydroelectrolytic imbalance. For instance, special relevance is given to the analysis of the inflammatory component of some forms of cell death over that of others, as an important and differential pathophysiological determinant. Finally, known molecular mechanisms and signalling pathways involved in each cell death type pose appropriate targets to specifically prevent or reverse AKI, provided that further knowledge of their participation and repercussion in each AKI syndrome is progressively increased in the near future.

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Crossref · 10.1093/ckj/sfv069

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  • Kidney tissue is susceptible to ferroptosis, and ferroptosis inhibitors may help reduce kidney injury.

    “These results reinforce the susceptibility of kidney tissue to ferroptosis and suggest the value of ferroptosis inhibitors to ameliorate kidney injury [59].”

    From Ferroptosis: Death by Lipid Peroxidation (2016) · cites this paper as [59]

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Research works printed but not linked: 3

  1. [103]Linkermann A Bräsen JH Darding M Two independent pathways of regulated necrosis mediate ischemia-reperfusion injury. Proc Natl Acad Sci USA 2013; 110: 12024– 9 23818611 PMC3718149
  2. [122]Yoshida T Shimizu A Masuda Y Caspase-3-independent internucleosomal DNA fragmentation in ischemic acute kidney injury. Nephron Exp Nephrol 2012; 120: e103– e113 22678593
  3. [140]Linkermann A Bräsen JH Himmerkus N Rip1 (receptor-interacting protein kinase 1) mediates necroptosis and contributes to renal ischemia/reperfusion injury. Kidney Int 2012; 81: 751– 761 22237751

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Authors
Sancho-Martínez, S. M., López-Novoa, J. M., & López-Hernández, F. J.
Affiliations
Universidad de Salamanca (ES)
Venue
Clinical Kidney Journal
Published
2015-08-25
Volume
8
Issue
5
Pages
548-559
ISSN
  • 2048-8505 (ISSN-L)
  • 2048-8513
OpenAlex
W2261452917
Cited by
130
References
142
Citations by year
2026: 5 · 2025: 14 · 2024: 18 · 2023: 10 · 2022: 13 · 2021: 9 · 2020: 12 · 2019: 14 · 2018: 14 · 2017: 8 · 2016: 11 · 2015: 2
FWCI
1.79
Type
journal article
Language
en
Open access
Locations
  • Clinical Kidney Journal (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Nephrology › Acute Kidney Injury Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Health Sciences › Medicine › Nephrology › Renal Diseases and Glomerulopathies
Keywords
acute kidney injury, apoptosis, necroptosis, parthanatos, autophagic cell death, mitotic catastrophe, tubular necrosis, glomerular filtration, azotemia, inflammation, signaling pathways, AKI prevention

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