Pathophysiological role of different tubular epithelial cell death modes in acute kidney injury
Open accessAbstract
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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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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Ferroptosis: Death by Lipid Peroxidation
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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
- Publisher
- Oxford University Press (OUP)
- Published
- 2015-08-25
- Volume
- 8
- Issue
- 5
- Pages
- 548-559
- ISSN
- 2048-8505 (ISSN-L)
- 2048-8513
- PMC
- PMC4581387
- 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
- gold
- doi.org
- 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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